ORIGINAL_ARTICLE
The Effects of Dental Pulp Stem Cell Conditioned Media on the Proliferation of Peripheral Blood Mononuclear Cells
Background: Dental Pulp Stem Cells (DPSCs) are multipotent mesenchymal stem cells. DPSCs can renew themselves and differentiate into various cell types such as adipocytes, osteocytes, neurons, etc. DPSCs possess immunomodulatory properties and can inhibit peripheral blood mononuclear cell (PBMC) proliferation. Recent studies showed that conditioned-medium mesenchymal stem cells also had immunosuppressive activity. The ability of DPSC conditioned medium to suppress proliferation of allogeneic PBMC determined using BrdU (5-bromo-2’-deoxyuridine) proliferation assay. Materials and Methods: Dental pulp stem cells were extracted from a wisdom tooth. These cells are characterized for differentiation potential to adipogenic and osteogenic lineage and expression of mesenchymal stem cells markers, including CD105, CD73, CD90, CD14, CD-34, and CD45. The characterized DPSCs were cultured, and the conditioned medium (CM) got isolated. Stimulated and non-stimulated PBMCs from the allogeneic donor were cultured with DPSC-CM for 24, 48, and 72 hours. The proliferation of PBMCs was measured with BrdU assay. Results: The BrdU test results showed that DPSC-CM reduced allogeneic PBMC proliferation at different time points. DPSC-CM could inhibit stimulated and non-stimulated PBMC in 48 and 72 hours after incubation.Conclusion: This study demonstrated that DPSC-CM had an immunomodulatory effect on the proliferation of allogeneic cells.
https://immunoreg.shahed.ac.ir/article_918_d56dc1e6f676594dcb199beb64aab66d.pdf
2020-01-01
69
74
10.32598/Immunoregulation.1.4.187
Dental pulp stem cell
Immunomodulatory
Conditioned medium
Stem cell
Nikoo
Hossein-Khannazer
nikoo.khannazer@gmail.com
1
Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Seyed Mahmoud
Hashemi
smmhashemi@sbmu.ac.ir
2
Department of Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Saeed
Namaki
saeed.namaki@yahoo.com
3
Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Mandana
Sattari
mandanasattari@yahoo.com
4
Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Arash
Khojasteh
arashkhojasteh@sbmu.ac.ir
5
Department of Tissue Engineering and Applied Cell Sciences, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
LEAD_AUTHOR
Waddington RJ, Youde SJ, Lee CP, Sloan AJ. Isolation of distinct progenitor stem cell populations from dental pulp. 2009; 268-74. [DOI:10.1159/000151447] [PMID]
1
Gronthos S, Mankani M, Brahim J, Robey PG, Shi S. Postnatal human Dental Pulp Stem Cells (DPSCs) in vitro and in vivo. Proceedings of the National Academy of Sciences of the United States of America. 2000; 97(25):13625-30. [DOI:10.1073/pnas.240309797] [PMID] [PMCID]
2
Rodriguez-Lozano FJ, Bueno C, Insausti CL, Meseguer L, Ramirez MC, Blanquer M, et al. Mesenchymal stem cells derived from dental tissues. International Endodontic Journal. 2011; 44(9):800-6. [DOI:10.1111/j.1365-2591.2011.01877.x] [PMID]
3
Howard C, Murray PE, Namerow KN. Dental pulp stem cell migration. International Endodontic Journal. 2010; 36(12):1963-6. [DOI:10.1016/j.joen.2010.08.046] [PMID]
4
Kawashima N. Characterisation of dental pulp stem cells: A new horizon for tissue regeneration. Archives of Oral Biology. 2012; 57(11):1439-58. [DOI:10.1016/j.archoralbio.2012.08.010] [PMID]
5
Kerkis I, Caplan AI. Stem cells in dental pulp of deciduous teeth. Tissue Engineering Part B: Reviews. 2012; 18(2):129-38. [DOI:10.1089/ten.teb.2011.0327] [PMID] [PMCID]
6
Huang AH-C, Chen Y-K, Lin L-M, Shieh T-Y, Chan AW-S. Isolation and characterization of dental pulp stem cells from a supernumerary tooth. Journal of Oral Pathology & Medicine. 2008; 37(9):571-4. [DOI:10.1111/j.1600-0714.2008.00654.x] [PMID]
7
Arthur A, Rychkov G, Shi S, Kolbar SA, Gronthos. Adult human dental pulp stem cells differentiate toward functionally active neurons under appropriate environmental cues. International Journal of Stem Cells. 2008; 26(7):1787-95. [DOI:10.1634/stemcells.2007-0979] [PMID]
8
Li Z, Jiang CM, An S, Cheng Q, Huang YF, Wang YT, et al. Immunomodulatory properties of dental tissue-derived mesenchymal stem cells. Oral Diseases. 2014; 20(1):25-34. [DOI:10.1111/odi.12086] [PMID]
9
Demircan PC, Sariboyaci AE, Unal ZS, Gacar G, Subasi C, Karaoz E. Immunoregulatory effects of human dental pulp-derived stem cells on T cells: Comparison of transwell co-culture and mixed lymphocyte reaction systems. Cytotherapy. 2011; 13(10):1205-20. [DOI:10.3109/14653249.2011.605351] [PMID]
10
Lei M, Li K, Li B, Gao L-N, Chen F-M, Jin Y. Mesenchymal stem cell characteristics of dental pulp and periodontal ligament stem cells after in vivo transplantation. Biomaterials. 2014; 35(24):6332-43. [DOI:10.1016/j.biomaterials.2014.04.071] [PMID]
11
Leprince JG, Zeitlin BD, Tolar M, Peters OA. Interactions between immune system and mesenchymal stem cells in dental pulp and periapical tissues. 2012; 689-701. [DOI:10.1111/j.1365-2591.2012.02028.x] [PMID]
12
Walter MNM, Wright KT, Fuller HR, MacNeil S, Johnson WEB. Mesenchymal stem cell-conditioned medium accelerates skin wound healing: An in vitro study of fibroblast and keratinocyte scratch assays. Experimental Cell Research. 2010; 316(7):1271-81. [DOI:10.1016/j.yexcr.2010.02.026] [PMID]
13
Timmers L, Lim SK, Hoefer IE, Arslan F, Lai RC, van Oorschot AAM, et al. Human mesenchymal stem cell-conditioned medium improves cardiac function following myocardial infarction. Stem Cell Research. 2011; 6(3):206-14. [DOI:10.1016/j.scr.2011.01.001] [PMID]
14
Hossein-khannazer N, Mahmoud S, Namaki S. Study of the immunomodulatory effects of osteogenic differentiated human dental pulp stem cells. Life Sciences. 2019; 216(1):111-8. [DOI:10.1016/j.lfs.2018.11.040] [PMID]
15
Tang R, Wei F, Wei L, Wang S, Ding G. Osteogenic differentiated periodontal ligament stem cells maintain their immunomodulatory capacity. Journal of Tissue Engineering and Regenerative Medicine. 2014; 8(3):226-32. [DOI:10.1002/term.1516] [PMID]
16
Kay AG, Long G, Tyler G, Stefan A, Broadfoot SJ, Piccinini AM, et al. Mesenchymal stem cell-conditioned medium reduces disease severity and immune responses in inflammatory arthritis. Scientific Reports. 2017; 1-11. [DOI:10.1038/s41598-017-18144-w] [PMID] [PMCID]
17
Li M, Luan F, Zhao Y, Hao H, Liu J, Dong L, et al. Mesenchymal stem cell-conditioned medium accelerates wound healing with fewer scars. International Wound Journal. 2017; 14(1):64-73. [DOI:10.1111/iwj.12551] [PMID]
18
Yamaguchi S, Shibata R, Yamamoto N, Nishikawa M, Hibi H, Tanigawa T, et al. Dental pulp-derived stem cell conditioned medium reduces cardiac injury following ischemia-reperfusion. Scientific Reports. 2015; 5:16295. [DOI:10.1038/srep16295] [PMID] [PMCID]
19
ORIGINAL_ARTICLE
Microencapsulated Saccharomyces Cerevisiae Var. Boulardii and IgA Secretion From Intestinal Epithelia in Wistar Rats
Background: Probiotics are live microorganisms with many health benefits for their host. The intestinal microbiota are the largest source of microbial variation and plays a significant role in host responses in health and disease. However, few studies have assessed the repercussions of probiotics regarding the morphology and immunology of the gastrointestinal tract in animal models. This study was designed to evaluate the effect of administering capsulated Saccharomyces species on gastrointestinal tract properties in rats. Materials and Methods: In this study mice rats were feed with Saccharomyces Boulardii intwo forms of capsulated and free. IgA was measured in duodenal and jejunal washings using ELISA assay according to the manufacturer’s instructions.Results: Probiotic S. boulardii could increase IgA secretion from duodenum and jejunum in comparison with the control group, and this increase was significant in microencapsulated S.boulardii-treated group and in the duodenum of S. boulardii-treated group (PConclusion: It can be concluded that S. boulardii is a potential probiotic yeast with immunostimulatory effects which can be used in the treatment of gastrointestinal disorders.
https://immunoreg.shahed.ac.ir/article_932_788d794d06120bcd45c0d6dc1bddd5db.pdf
2020-01-01
75
78
10.32598/Immunoregulation.1.4.193
Probiotic
IgA
Intestine
Zohreh
Farahnejad
zfarahnejad@yahoo.com
1
Department of Medical Mycology, School of Medicine, AJA University of Medical Sciences, Tehran, Iran.
AUTHOR
Donya
Nikaein
donya.nik@gmail.com
2
Mycology Research Center, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran.
AUTHOR
Ali Reza
Khosravi
khosravialir@gmail.com
3
Mycology Research Center, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran.
AUTHOR
Reza
Rahmani
r.rahmani_dvm@yahoo.com
4
Department of Clinical Biochemistry, School of Medicine, Tehran University of medical science , Tehran, Iran.
AUTHOR
Hassan
Ghorbani-Choboghlo
hghorbani67@ut.ac.ir
5
Mycology Research Center, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran.
LEAD_AUTHOR
Qamar A, Aboudola S, Warny M, Michetti P, Pothoulakis C, LaMont J. Saccharomyces boulardii stimulates intestinal immunoglobulin A immune response to Clostridium difficiletoxin A in mice. Infection and Immunity. 2001; 69(4):2762-5. [DOI:10.1128/IAI.69.4.2762-2765.2001] [PMID] [PMCID]
1
Ritchie ML, Romanuk TN. A meta-analysis of probiotic efficacy for gastrointestinal diseases. PLOS One. 2012; 7(4):e34938. [DOI: 10.1371/journal.pone.0034938] [PMID] [PMCID]
2
Buts JP, Bernasconi P, Vaerman JP, Dive C. Stimulation of secretory IgA and secretory component of immunoglobulins in small intestine of rats treated with Saccharomyces boulardii. Digestive Diseases and Sciences. 1990; 35(2):251-6. [DOI:10.1007/BF01536771] [PMID]
3
Angelakis E. Weight gain by gut microbiota manipulation in productive animals. Microbial Pathogenesis. 2017; 106:162-70. [DOI:10.1016/j.micpath.2016.11.002]
4
Cruchet S, Furnes R, Maruy A, Hebel E, Palacios J, Medina F, et al. The use of probiotics in pediatric gastroenterology: A review of the literature and recommendations by Latin-American experts. Pediatric Drugs. 2015; 17(3):199-216. [DOI:10.1007/s40272-015-0124-6] [PMID] [PMCID]
5
Elmer GW, Surawicz CM, McFarland LV. Biotherapeutic agents: A neglected modality for the treatment and prevention of selected intestinal and vaginal infections. The Journal of the American Medical Association. 1996; 275(11):870-6. [DOI:10.1001/jama.275.11.870] [PMID]
6
Dias DR, Botrel DA, De Barros Fernandes RV, Borges SV. Encapsulation as a tool for bioprocessing of functional foods. Current Opinion in Food Science. 2017; 13:31-7. [DOI:10.1016/j.cofs.2017.02.001]
7
Lacroix C, Grattepanche F, Doleyres Y, Bergmaier D. Immobilised cell technologies for the dairy industry. In: NedovićRonnie V, Willaert R, editors. Applications of Cell Immobilisation Biotechnology. Dordrecht: Springer; 2005. [DOI:10.1007/1-4020-3363-X_18]
8
Shah NP, Ravula RR. Microencapsulation of probiotic bacteria and their survival in frozen fermented dairy desserts. Australian Journal of Dairy Technology. 2000; 55(3):139-44.
9
Abdolhosseinzadeh E, Dehnad AR, Pourjafar H, Homayouni A, Ansari F. The production of probioticscallion yogurt: Viability of lactobacillus acidophilus freelyand microcapsulated in the product. Carpathian Journal of Food Science & Technology. 2018; 10(3):72-80.
10
Lim TS, Messiha N, Watson RR. Immune components of the intestinal mucosae of ageing and protein deficient mice. Immunology. 1981; 43(3):401-7. [PMID] [PMCID]
11
Ghorbani-Choboghlo H, Zahraei-Salehi T, Ashrafi-Helan J, Yahyaraeyat R, Pourjafar H, Nikaein D, et al. Microencapsulation of saccharomyces cerevisiae and its evaluation to protect in simulated gastric conditions. Iranian Journal of Microbiology. 2015; 7(6):338-42. [PMID] [PMCID]
12
Szajewska H, Kołodziej M. Systematic review with meta‐analysis: Saccharomyces boulardii in the prevention of antibiotic‐associated diarrhoea. Alimentary Pharmacology & Therapeutics. 2015; 42(7):793-801. [DOI:10.1111/apt.13344] [PMID]
13
Stier H, Bischoff SC. Influence of saccharomyces boulardii CNCM I-745on the gut-associated immune system. Clinical and Experimental Gastroenterology. 2016; 9:269-79. [DOI:10.2147/CEG.S111003] [PMID] [PMCID]
14
Hudson LE, McDermott CD, Stewart TP, Hudson WH, Rios D, Fasken MB, et al. Characterization of the probiotic yeast Saccharomyces boulardii in the healthy mucosal immune system. PLOS One. 2016; 11(4):e0153351. [DOI:10.1371/journal.pone.0153351] [PMID] [PMCID]
15
ORIGINAL_ARTICLE
Association of Nitric Oxide With Delayed Skin Problems After Sulfur Mustard Exposure: Part of Sardasht-Iran Cohort Study
Background: Exposure to Sulfur Mustard (SM) leads to short- and long-term adverse effects on various organs, including the skin. Despite several studies on long-term clinical manifestations of skin toxicity in SM-exposed individuals, the pathogenesis of SM-induced skin disorders is not fully understood. Materials and Methods: As part of Sardasht-Iran Cohort Study (SICS), this study aimed to find out the possibility of any correlation between the serums level of Nitric Oxide (NO) and skin problems due to the long-term effect of SM as well as the kind of skin illness. In this historical cohort study, 372 male SM-exposed subjects and 128 age-matched unexposed controls were studied. Clinical evaluation was carried out for all participants, and their serum concentration of NO was measured. Results: According to our results, the Mean±SD serum level of NO in the exposed group with skin disorders were significantly higher than that in the exposed group without skin disorders (1483.00±488.754µg/mL vs. 1364.50±487.887µg/mL; P=0.024). Also, among the exposed group, there was a significant elevation of serum NO associated with the type of lesion. For ezxample, specific lesions like mustard scar were associated with higher levels of NO compared to non-specific lesions like xerosis, itching, seborrheic dermatitis, etc. Also, a significant elevation in serum NO levels was found in the exposed subjects with pigmentation disorders (both hypo- and hyper-pigmentation) compared to the exposed participants without these skin problems (PConclusion: Our results show the highest serum level of NO in the exposed group with specific lesions and the lowest or normal level of NO in the unexposed group with no skin illness. The elevated serum levels of NO may be associated with the progression of some skin complications in the SM-exposed subjects. This finding serves as a basis for further research on the molecular mechanisms and pathways involved in the pathogenesis of skin disorders in SM-exposed patients.
https://immunoreg.shahed.ac.ir/article_919_38089e67ad98a0f1d388df07fc7917e6.pdf
2020-01-01
79
88
10.32598/Immunoregulation.1.4.197
Mustard gas
Skin
Nitric oxide
Cohort study
Nayere
Askari
askari.nr@gmail.com
1
Department of Biology, Faculty of Science, Shahid Bahonar University of Kerman, Kerman, Iran.
AUTHOR
Shohreh
Jalaie
2
Department of Epidemiology and Biostatistics, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
AUTHOR
Athar
Moin
3
Immunoregulation Research Center, Shahed University, Tehran, Iran.
AUTHOR
Seyed Naser
Emadi
4
Department of Dermatology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
AUTHOR
Ali
Khamesipour
khamesipour@tums.ac.ir
5
Center for Research and Training in Skin Diseases and Leprosy, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.
AUTHOR
Seyed Emad
Emadi
6
Mazandaran University of Medical Sciences, Sari, & Iranian Red Crescent Society, Tehran, Iran.
AUTHOR
Elham
Faghihzadeh
7
Immunoregulation Research Center, Shahed University, Tehran, Iran.
AUTHOR
Tooba
Ghazanfari
tghazanfari@yahoo.com
8
Immunoregulation Research Center, Shahed University, Tehran, Iran.
LEAD_AUTHOR
Ghazanfari T, Faghihzadeh S, Aragizadeh H, Soroush MR, Yaraee R, Mohammad Hassan Z, et al. Sardasht, Iran cohort study of chemical warfare victims: Design and methods. Archives of Iranian Medicine. 2009; 12(1):5-14.
1
Moin A, Ghazanfari T, Davoudi SM, Emadi N, Panahi Y, Hassan ZM, et al. Long-term skin findings of sulfur mustard exposure on the civilians of Sardasht, Iran. Toxin Reviews. 2009; 28(1):24-9. [DOI:10.1080/15569540802689311]
2
Emadi SN, Babamahmoodi F, Poursaleh Z, Sayad-Noori SS, Soroush MR, Maleki AR, et al. Sézary syndrome, Kaposi sarcoma and generalized dermato-phytosis 15 years after sulfur mustard gas exposure. Journal of Dermatological Case Reports. 2012; 6(3):86-9. [DOI:10.3315/jdcr.2012.1109] [PMID] [PMCID]
3
Poursaleh Z, Ghanei M, Babamahmoodi F, Izadi M, Harandi AA, Emadi SE, et al. Pathogenesis and treatment of skin lesions caused by sulfur mustard. Cutaneous and Ocular Toxicology. 2012; 31(3):241-9. [DOI:10.3109/15569527.2011.636119] [PMID]
4
Momeni AZ, Enshaeih S, Meghdadi M, Amindjavaheri M. Skin manifestations of mustard gas: A clinical study of 535 patients exposed to mustard gas. Archives of Dermatology. 1992; 128(6):775-80. [DOI:10.1001/archderm.1992.01680160059004]
5
Gröne A. Keratinocytes and cytokines. Veterinary Immunology and Immunopathology. 2002; 88(1):1-12. [DOI:10.1016/S0165-2427(02)00136-8]
6
Balkwill FR. Tumour necrosis factor. British Medical Bulletin. 1989; 45(2):389-400. [DOI:10.1093/oxfordjournals.bmb.a072330] [PMID]
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Bruch-Gerharz D, Ruzicka T, Kolb-Bachofen V. Nitric oxide and its implications in skin homeostasis and disease: A review. Archives of Dermatological Research. 1998; 290(12):643-51. [DOI:10.1007/s004030050367] [PMID]
8
Greaves M. Pruritus. In: Bolognia JL, Jorizzo J, Rapini R, eds. Dermatology. Edinburgh: Mosby; 2003.
9
Cals-Grierson M-M, Ormerod A. Nitric oxide function in the skin. Nitric Oxide. 2004; 10(4):179-93. [DOI:10.1016/j.niox.2004.04.005] [PMID]
10
Andoh T, Kuraishi Y. Nitric oxide enhances substance P-induced itch-associated responses in mice. British Journal of Pharmacology. 2003; 138(1):202-8. [DOI:10.1038/sj.bjp.0705004] [PMID] [PMCID]
11
Ghazanfari T, Sharifnia Z, Yaraee R, Pourfarzam S, Kariminia A, Mahlojirad M, et al. Serum soluble Fas ligand and nitric oxide in long-term pulmonary complications induced by sulfur mustard: Sardasht-Iran Cohort Study. International Immunopharmacology. 2009; 9(13):1489-93. [DOI:10.1016/j.intimp.2009.08.019] [PMID]
12
Green LC, Wagner DA, Glogowski J, Skipper PL, Wishnok JS, Tannenbaum SR. Analysis of nitrate, nitrite, and [15N]nitrate in biological fluids. Analytical Biochemistry. 1982; 126(1):131-8. [DOI:10.1016/0003-2697(82)90118-X]
13
Emadi SN, Aslani J, Poursaleh Z, Izadi M, Soroush M, Kafashi M, et al. Comparison late cutaneous complications between exposure to sulfur mustard and nerve agents. Cutaneous and Ocular Toxicology. 2012; 31(3):214-9. [DOI:10.3109/15569527.2011.641196] [PMID]
14
Moin A, Khamesipour A, Hassan ZM, Ebtekar M, Davoudi S-M, Vaez-Mahdavi M-R, et al. Pro-inflammatory cytokines among individuals with skin findings long-term after sulfur mustard exposure: Sardasht-Iran Cohort Study. International immunopharmacology. 2013; 17(3):986-90. [DOI:10.1016/j.intimp.2012.12.022] [PMID]
15
Schallreuter KU, Wood JM. Free radical reduction in the human epidermis. Free Radical Biology and Medicine. 1989; 6(5):519-32. [DOI:10.1016/0891-5849(89)90045-2]
16
Kohen R, Fanberstein D, Tirosh O. Reducing equivalents in the aging process. Archives of Gerontology and Geriatrics. 1997; 24(2):103-23. [DOI:10.1016/S0167-4943(96)00744-3]
17
Weller R. Nitric oxide: A key mediator in cutaneous physiology. Clinical and Experimental Dermatology. 2003; 28(5):511-4. [DOI:10.1046/j.1365-2230.2003.01365.x] [PMID]
18
Emadi SN, Kaffashi M, Poursaleh Z, Akhavan-Moghaddam J, Soroush MR, Emadi SE, Taghavi NO. Sulfur mustard-induced poikiloderma: A case report. Cutaneous and Ocular Toxicology. 2011; 30(2):170-4. [DOI:10.3109/15569527.2010.539585] [PMID]
19
Roméro-Graillet C, Aberdam E, Clément M, Ortonne J-P, Ballotti R. Nitric oxide produced by ultraviolet-irradiated keratinocytes stimulates melanogenesis. Journal of Clinical Investigation. 1997; 99(4):635-42. [DOI:10.1172/JCI119206] [PMID] [PMCID]
20
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22
Smith KJ, Hurst CG, Moeller RB, Skelton HG, Sidell FR. Sulfur mustard: Its continuing threat as a chemical warfare agent, the cutaneous lesions induced, progress in understanding its mechanism of action, its long-term health effects, and new developments for protection and therapy. Journal of the American Academy of Dermatology. 1995; 32(5):765-76. [DOI:10.1016/0190-9622(95)91457-9]
23
Koca R, Armutcu F, Altinyazar H, Gürel A. Oxidant‐antioxidant enzymes and lipid peroxidation in generalized vitiligo. Clinical and Experimental Dermatology. 2004; 29(4):406-9. [DOI:10.1111/j.1365-2230.2004.01524.x] [PMID]
24
Murohara T, Witzenbichler B, Spyridopoulos I, Asahara T, Ding B, Sullivan A, et al. Role of endothelial nitric oxide synthase in endothelial cell migration. Arteriosclerosis, Thrombosis, and Vascular Biology. 1999; 19(5):1156-61. [DOI:10.1161/01.ATV.19.5.1156]
25
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26
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27
Askari N, Vaez-Mahdavi M-R, Moaiedmohseni S, Khamesipour A, Soroush M-R, Moin A, et al. Association of chemokines and prolactin with cherry angioma in a sulfur mustard exposed population-Sardasht-Iran cohort study. International immunopharmacology. 2013;17(3):991-5. [DOI:10.1016/j.intimp.2012.12.016] [PMID]
28
Hon K, Leung T, Kam W, Lam M, Wong K, Yung E, et al. Exhaled nitric oxide levels are not correlated with eczema severity in Chinese children with atopic dermatitis. Journal of Asthma. 2006;43(6):417-9. [DOI:10.1080/02770900600701341] [PMID]
29
Devenney I, Norrman G, Forslund T, Fälth-Magnusson K, Sundqvist T. Urinary nitric oxide excretion in infants with eczema. Pediatric Allergy and Immunology. 2010;21(1-Part-II):e229-e34. [DOI:10.1111/j.1399-3038.2009.00892.x] [PMID]
30
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31
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32
Emadi SN, Moeineddin F, Sorush MR. Urinary and cutaneous complications of sulphur mustard poisoning preceding pulmonary and ocular involvement: an unusual sequence of symptoms. Clin Exp Dermatol 2009, 34, e7-10. [DOI:10.1111/j.1365-2230.2008.02965.x] [PMID]
33
Emadi SN, Hosseini-Khalili A, Soroush M, Ardakani MK,Ghassemi-Broumand M, Davoodi SM, et al. External ure- thral stenosis: a latent effect of sulfur mustard two decades postexposure.Int J Dermatol 2009; 48(9):960-963. [DOI:10.1111/j.1365-4632.2009.04128.x] [PMID]
34
Viera MH, Amini S, Valins W, Berman B. Innovative therapies in the treatment of keloids and hypertrophic scars. The Journal of Clinical and Aesthetic Dermatology. 2010; 3(5):20-6. [PMID] [PMCID]
35
ORIGINAL_ARTICLE
Immunoregulatory Properties of Arteether in Folic Acid-Chitosan-Fe3O4 Composite Nanoparticle in 4T1 Cell Line and Mice Bearing Breast Cancer
Background: Many studies have focused on the potent anti-cancer activity of Arteether (ARE). However, the hydrophobic property of this drug limits its application. To increase the bioavailability of ARE, we formulated a Nanosystem (NS) of Folic Acid (FA), Chitosan (CS), and Fe3O4 for delivery of ARE into breast cancer. Materials and Methods: The CS-coated Fe3O4 was synthesized by co-precipitation of Fe2+ and Fe3+ in CS gel-like solution. Then, it was conjugated with FA and ARE. The properties of ARE loaded Nanoparticles (NPs) were characterized by Dynamic Light Scattering (DLS), Fourier Transform-Infrared (FTIR) spectra, Scanning Electron Microscopy (SEM), drug loading efficiency, and drug release. The bioactivity of this complex was evaluated in vitro and in vivo settings. Tumor volume was measured, and the cytokines of Interferon-gamma IFN-γ and interleukin 4 (IL-4) were assessed in mice splenocytes. Results: DLS showed an average size of 198nm and the charge of about -7mV. FTIR confirmed the formation of ARE loaded NPs and SEM indicated its solid, dense structure. The drug exhibited a loading capacity of (20%) and significant release in citrate buffer with pH 5.4 compared with phosphate-buffered saline with pH 7.4. The NS showed significant inhibitory effect on the growth of 4T1 cell line and tumor volume. It also augmented IFN-γ and IL-4 production in breast cancer-bearing mice. ARE in FA-CS-Fe3O4 composite NPs may significantly suppress tumor growth. Conclusion: This NS can be utilized in the nano-based drug delivery system for the treatment of breast cancer.
https://immunoreg.shahed.ac.ir/article_925_14bc04581ee64d0f500de5e4e8226d02.pdf
2020-01-01
89
102
10.32598/Immunoregulation.1.4.207
Arteether
Nanosystem
Chitosan
Folic acid
Breast cancer
Hajar
Rajaei
hajar.rajaee@modares.ac.ir
1
Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
AUTHOR
Mirza Ali
Mofazzal Jahromi
alimofazzal@yahoo.com
2
Department of Advanced Medical Sciences and Technologies, School of Medicine, Jahrom University of Medical Sciences, Shiraz, Iran.
AUTHOR
Nima
Khoramabadi
nimakhoramabadi@modares.ac.ir
3
Department of Bacteriology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
AUTHOR
Zuhair
Mohammad Hassan
hasan_zm@modares.ac.ir
4
Department of Immunology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
LEAD_AUTHOR
Ghazanfari T, Faghihzadeh S, Aragizadeh H, Soroush MR, Yaraee R, Mohammad Hassan Z, et al. Sardasht, Iran cohort study of chemical warfare victims: Design and methods. Archives of Iranian Medicine. 2009; 12(1):5-14.
1
Moin A, Ghazanfari T, Davoudi SM, Emadi N, Panahi Y, Hassan ZM, et al. Long-term skin findings of sulfur mustard exposure on the civilians of Sardasht, Iran. Toxin Reviews. 2009; 28(1):24-9. [DOI:10.1080/15569540802689311]
2
Emadi SN, Babamahmoodi F, Poursaleh Z, Sayad-Noori SS, Soroush MR, Maleki AR, et al. Sézary syndrome, Kaposi sarcoma and generalized dermato-phytosis 15 years after sulfur mustard gas exposure. Journal of Dermatological Case Reports. 2012; 6(3):86-9. [DOI:10.3315/jdcr.2012.1109] [PMID] [PMCID]
3
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4
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14
Moin A, Khamesipour A, Hassan ZM, Ebtekar M, Davoudi S-M, Vaez-Mahdavi M-R, et al. Pro-inflammatory cytokines among individuals with skin findings long-term after sulfur mustard exposure: Sardasht-Iran Cohort Study. International immunopharmacology. 2013; 17(3):986-90. [DOI:10.1016/j.intimp.2012.12.022] [PMID]
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18
Emadi SN, Kaffashi M, Poursaleh Z, Akhavan-Moghaddam J, Soroush MR, Emadi SE, Taghavi NO. Sulfur mustard-induced poikiloderma: A case report. Cutaneous and Ocular Toxicology. 2011; 30(2):170-4. [DOI:10.3109/15569527.2010.539585] [PMID]
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22
Smith KJ, Hurst CG, Moeller RB, Skelton HG, Sidell FR. Sulfur mustard: Its continuing threat as a chemical warfare agent, the cutaneous lesions induced, progress in understanding its mechanism of action, its long-term health effects, and new developments for protection and therapy. Journal of the American Academy of Dermatology. 1995; 32(5):765-76. [DOI:10.1016/0190-9622(95)91457-9]
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24
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25
Verma S, Wang C-H, Li S-H, Dumont AS, Fedak PW, Badiwala MV, et al. A self-fulfilling prophecy C-reactive protein attenuates nitric oxide production and inhibits angiogenesis. Circulation. 2002;106(8):913-9. [DOI:10.1161/01.CIR.0000029802.88087.5E] [PMID]
26
Nakagawa T, Sato W, Glushakova O, Heinig M, Clarke T, Campbell-Thompson M, et al. Diabetic endothelial nitric oxide synthase knockout mice develop advanced diabetic nephropathy. Journal of the American Society of Nephrology. 2007;18(2):539-50. [DOI:10.1681/ASN.2006050459] [PMID]
27
Askari N, Vaez-Mahdavi M-R, Moaiedmohseni S, Khamesipour A, Soroush M-R, Moin A, et al. Association of chemokines and prolactin with cherry angioma in a sulfur mustard exposed population-Sardasht-Iran cohort study. International immunopharmacology. 2013;17(3):991-5. [DOI:10.1016/j.intimp.2012.12.016] [PMID]
28
Hon K, Leung T, Kam W, Lam M, Wong K, Yung E, et al. Exhaled nitric oxide levels are not correlated with eczema severity in Chinese children with atopic dermatitis. Journal of Asthma. 2006;43(6):417-9. [DOI:10.1080/02770900600701341] [PMID]
29
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30
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31
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32
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33
Emadi SN, Hosseini-Khalili A, Soroush M, Ardakani MK,Ghassemi-Broumand M, Davoodi SM, et al. External ure- thral stenosis: a latent effect of sulfur mustard two decades postexposure.Int J Dermatol 2009; 48(9):960-963. [DOI:10.1111/j.1365-4632.2009.04128.x] [PMID]
34
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35
ORIGINAL_ARTICLE
Serum Levels of Interleukin-10 and Tumor Growth Factor-β1 in Children With Eosinophilic Gastrointestinal Disorders Compared to Control Groups
Background: Eosinophilic Gastrointestinal Disorders (EGID) are a heterogeneous group of gastrointestinal disorders, associated with an increase of the eosinophils in the gastrointestinal mucosal tissue. Regulatory T cells (Tregs), as a subset of T cells, have a proven prominent role in immunopathology and protection against allergic diseases. Also, they appear to play a role in EGID pathogenesis. In the present study, serum levels of Tumor Growth Factor (TGF)-β and interleukin (IL)-10 were measured in patients with EGID compared to patients with Gastroesophageal Reflux Disease (GERD) and healthy subjects.Materials and Methods: A total of 34 patients with EGID, 23 with GERD, and 25 healthy controls were included in the study. The diagnoses of EGID and GERD were made based on the patients’ clinical symptoms, endoscopic findings, and biopsy confirmation. A questionnaire of demographic information, allergy history, as well as endoscopic-pathological and skin prick test results were completed and performed. The serum levels of TGF-β and IL-10 were measured using the ELISA method. Results: Family history of allergic disorders in patients with EGID or GERD was significantly high compared to healthy controls (P=0.010, P=0.005, respectively). There was a statistically significant increase in serum levels of TGF-β1 (P=0.025), but no significant difference was observed in serum level of IL-10 among three groups. However, the serum level of IL-10 was significantly high in a subgroup of patients with upper gastrointestinal eosinophilic involvement compared to the healthy controls (P=0.018).Conclusion: Significant increase in the serum level of IL-10 and TGF- β might be due to the Tregs dysfunction in EGID patients. Further studies should determine the role of Tregs in the pathogenesis of EGID.
https://immunoreg.shahed.ac.ir/article_928_d815d0dbed1bb4ee75d603f1d217726b.pdf
2020-01-01
103
110
10.32598/Immunoregulation.1.4.221
Eosinophilic gastrointestinal disorders (EGID)
Gastroesophageal reflux disease (GERD)
Tumor growth factor (TGF)-β
Interleukin (IL)-10
Eosinophilic Esophagitis
Delara
Babaie
delara77@yahoo.com
1
Pediatric Pathology Research Center, Research Institute for Children’s Health, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Zahra
Daneshmandi
danesmandiz@gmail.com
2
Department of Allergy and Clinical Immunology, Mofid Children’s Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Sara
Jafarian
sara.jafarian79@yahoo.com
3
Department of Allergy and Clinical Immunology, Mofid Children’s Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Zahra
Chavoshzadeh
zahra_chavoshzadeh@yahoo.com
4
Department of Allergy and Clinical Immunology, Mofid Children’s Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Shima
Rsouli
sh.rasouli.1984@gmail.com
5
Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Mahboubeh
Mansouri
mbmans65@gmail.com
6
Department of Allergy and Clinical Immunology, Mofid Children’s Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Aliakbar
Sayyari
sayyari@yahoo.com
7
Pediatric Gastroenterology, Hepatology and Nutrition Research Center, Research Institute for Children’s Health, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Farid
Imanzadeh
imanzade@yahoo.com
8
Pediatric Gastroenterology, Hepatology and Nutrition Research Center, Research Institute for Children’s Health, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Naghi
Dara
naghidara@yahoo.com
9
Pediatric Gastroenterology, Hepatology and Nutrition Research Center, Research Institute for Children’s Health, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Pejman
Rouhani
p.rouhani@yahoo.com
10
Pediatric Gastroenterology, Hepatology and Nutrition Research Center, Research Institute for Children’s Health, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Katayoun
Khatami
khatami.k@gmail.com
11
Pediatric Gastroenterology, Hepatology and Nutrition Research Center, Research Institute for Children’s Health, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Maryam
Kazemi-Aghdam
kazemiaghsam.m@yahoo.com
12
Pediatric Pathology Research Center, Research Institute for Children’s Health, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Yalda
Nilipour
yahlda_ni@yahoo.com
13
Pediatric Pathology Research Center, Research Institute for Children’s Health, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Maliheh
Khoddami
mali.khoddami@gmail.com
14
Pediatric Pathology Research Center, Research Institute for Children’s Health, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Reza
Gholami
reza.gholami@yahoo.com
15
Department of Gastroenterology, Taleghani Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Reihane
Motaghinezhad
16
Department of Allergy and Clinical Immunology, Mofid Children’s Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Shima
Rasouli
17
Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
AUTHOR
Mehrnaz
Mesdaghi
mehrnaz_mesdaghi@yahoo.com
18
Department of Allergy and Clinical Immunology, Mofid Children’s Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
LEAD_AUTHOR
Rothenberg ME. Eosinophilic Gastrointestinal Disorders (EGID). Journal of Allergy and Clinical Immunology. 2004; 113(1):11-28. [DOI:10.1016/j.jaci.2003.10.047] [PMID]
1
Cianferoni A, Spergel JM. Eosinophilic esophagitis and gastroenteritis. Current Allergy and Asthma Reports. 2015; 15(9):58. [DOI:10.1007/s11882-015-0558-5] [PMID]
2
Kern E, Lin D, Larson A, Yang GY, Taft T, Zalewski A, et al. Prospective assessment of the diagnostic utility of esophageal brushings in adults with eosinophilic esophagitis. Diseases of the Esophagus. 2016; 29(1):48-53. [DOI:10.1111/dote.12304] [PMID]
3
Kia L, Hirano I. Distinguishing GERD from eosinophilic oesophagitis: Concepts and controversies. Nature Reviews Gastroenterology & Hepatology. 2015; 12(7):379-86. [DOI:10.1038/nrgastro.2015.75] [PMID] [PMCID]
4
Park H. An overview of eosinophilic esophagitis. Gut and Liver. 2014; 8(6):590-7. [DOI:10.5009/gnl14081] [PMID] [PMCID]
5
Fleisher T SW, Shroeder H, Frew A, Weyand C. Clinical immunology principles and practice, 4th edtion. Philadelphia: Elsivier, Saunder; 2013.
6
Rivas MN, Chatila TA. Regulatory T cells in allergic diseases. Journal of Allergy and Clinical Immunology. 2016; 138(3):639-52. [DOI:10.1016/j.jaci.2016.06.003] [PMID] [PMCID]
7
Fuentebella J, Patel A, Nguyen T, Sanjanwala B, Berquist W, Kerner JA, et al. Increased number of regulatory T cells in children with eosinophilic esophagitis. Journal of Pediatric Gastroenterology and Nutrition. 2010; 51(3):283-9. [DOI:10.1097/MPG.0b013e3181e0817b] [PMID]
8
Rothenberg ME. Eosinophilic gastrointestinal disorders. In: Adkinson NF, Bochner BS, Burks AW, Busse WW, Holgate ST, Lemanske RF, et al. (editors). Middleton’s Allergy (8th edition). London: Elsevier, Saunders; 2014.
9
Molina-Infante J, Arias A, Barrio J, Rodriguez-Sanchez J, Sanchez-Cazalilla M, Lucendo AJ. Four-food group elimination diet for adult eosinophilic esophagitis: A prospective multicenter study. Journal of Allergy and Clinical Immunology. 2014; 134(5):1093-9. [DOI:10.1016/j.jaci.2014.07.023] [PMID]
10
Kagalwalla AF, Amsden K, Shah A, Ritz S, Manuel-Rubio M, Dunne K, et al. Cow’s milk elimination: A novel dietary approach to treat eosinophilic esophagitis. Journal of Pediatric Gastroenterology and Nutrition. 2012; 55(6):711-6. [DOI:10.1097/MPG.0b013e318268da40] [PMID]
11
Spergel JM, Andrews T, Brown-Whitehorn TF, Beausoleil JL, Liacouras CA. Treatment of eosinophilic esophagitis with specific food elimination diet directed by a combination of skin prick and patch tests. Annals of Allergy, Asthma & Immunology. 2005; 95(4):336-43. [DOI:10.1016/S1081-1206(10)61151-9]
12
Spergel JM, Beausoleil JL, Mascarenhas M, Liacouras CA. The use of skin prick tests and patch tests to identify causative foods in eosinophilic esophagitis. Journal of Allergy and Clinical Immunology. 2002; 109(2):363-8. [DOI:10.1067/mai.2002.121458] [PMID]
13
Sherrill JD, Gao PS, Stucke EM, Blanchard C, Collins MH, Putnam PE, et al. Variants of thymic stromal lymphopoietin and its receptor associate with eosinophilic esophagitis. Journal of Allergy and Clinical Immunology. 2010; 126(1):160-5. [DOI:10.1016/j.jaci.2010.04.037] [PMID] [PMCID]
14
Ziegler SF, Artis D. Sensing the outside world: TSLP regulates barrier immunity. Nature Immunology. 2010; 11(4):289-93. [DOI:10.1038/ni.1852] [PMID] [PMCID]
15
Stuck MC, Straumann A, Simon HU. Relative lack of T regulatory cells in adult eosinophilic esophagitis: No normalization after corticosteroid therapy. Allergy. 2011; 66(5):705-7. [DOI:10.1111/j.1398-9995.2010.02525.x] [PMID]
16
Pohlers D, Brenmoehl J, Löffler I, Müller CK, Leipner C, Schultze-Mosgau S, et al. TGF-β and fibrosis in different organs: Molecular pathway imprints. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease. 2009; 1792(8):746-56. [DOI:10.1016/j.bbadis.2009.06.004] [PMID]
17
Hill DA, Spergel JM. The immunologic mechanisms of eosinophilic esophagitis. Current Allergy and Asthma Reports. 2016; 16(2):9. [DOI:10.1007/s11882-015-0592-3] [PMID] [PMCID]
18
Urban ML, Manenti L, Vaglio A. Fibrosis: A common pathway to organ injury and failure. The New England Journal of Medicine. 2015; 373(1):95-6. [DOI:10.1056/NEJMc1504848]
19
Frischmeyer-Guerrerio PA, Guerrerio AL, Oswald G, Chichester K, Myers L, Halushka MK, et al. TGFbeta receptor mutations impose a strong predisposition for human allergic disease. Science Translational Medicine. 2013; 5(195):195ra94. [DOI:10.1126/scitranslmed.3006448] [PMID] [PMCID]
20
Massague J. TGFbeta signalling in context. Nature Reviews Molecular Cell Biology. 2012; 13(10):616-30. [DOI:10.1038/nrm3434] [PMID] [PMCID]
21
Aceves SS, Newbury RO, Chen D, Mueller J, Dohil R, Hoffman H, et al. Resolution of remodeling in eosinophilic esophagitis correlates with epithelial response to topical corticosteroids. Allergy. 2010; 65(1):109-16. [DOI:10.1111/j.1398-9995.2009.02142.x] [PMID] [PMCID]
22
Arshi S, Babaie D, Nabavi M, Tebianian M, Ghalehbaghi B, Jalali F, et al. Circulating level of CD4+ CD25+ FOXP3+ T cells in patients with chronic urticaria. International Journal of Dermatology. 2014; 53(12):e561-6. [DOI:10.1111/ijd.12630] [PMID]
23
Babaie D, Nabavi M, Arshi S, Gorjipour H, Darougar S. The relationship between serum interleukin-6 level and chronic urticaria. Immunoregulation. 2018; 1(3):159-64. [DOI:10.32598/IMMUNOREGULATION.1.3.159]
24
Pellerin L, Jenks JA, Begin P, Bacchetta R, Nadeau KC. Regulatory T cells and their roles in immune dysregulation and allergy. Immunologic Research. 2014; 58(2-3):358-68. [DOI:10.1007/s12026-014-8512-5] [PMID] [PMCID]
25
Xystrakis E, Boswell SE, Hawrylowicz CM. T regulatory cells and the control of allergic disease. Expert Opinion on Biological Therapy. 2006; 6(2):121-33. [DOI:10.1517/14712598.6.2.121] [PMID]
26
ORIGINAL_ARTICLE
miR-320 and Inflammation Regulation in Experimental Autoimmune Encephalomyelitis Through Interference With Tumor Growth Factor-β Signaling Pathway
Background: MicroRNAs are small non-coding RNAs that regulate gene expression and involve in many cellular and physiological mechanisms. Recent studies have revealed that dysregulation of microRNAs might contribute to autoimmune disorders such as Multiple Sclerosis (MS). Based on these findings, we examined the potential role of miR-320 isoforms; miR-320-3p and miR-320-5p, in the context of autoimmune neuroinflammation and pathogenesis of EAE, which is an animal model of MS.Materials and Methods: The expression levels of miR-320-3p and miR-320-5p, and their predicted target genes, TGFBR2 and Smad2, were quantified in the CNS tissue in mice with Experimental Autoimmune Encephalomyelitis (EAE) using RT-PCR method. The expression was also examined in splenocytes macrophages and astrocytes. To examine the interaction of miR-320-3p and miR-320-5p with the 3′-UTR of potential target transcripts, the mimic sequences of both isoforms were transfected into splenocytes and then examined by RT-PCR. Results: The expression of both isoforms of miR-320 significantly increased in different phases of EAE and activated lymphocytes, whereas the levels of their predicted target genes, Smad2 and TGFBR2 decreased in these cells. Obtained data revealed that miR-320-5p level significantly increased in activated macrophages and astrocytes; however, the miR320-3p level did not show significant changes in these cells after Lipopolysaccharide (LPS) stimulation. The levels of TGFBR2 and Smad2 decreased in transfected splenocytes.Conclusion: Our findings suggest that upregulation of miR-320 isoforms might be involved in the neuroinflammation and pathogenesis of MS through targeting and suppression of TGFBR2 and Smad2, i.e. protective genes in MS.
https://immunoreg.shahed.ac.ir/article_929_dcb09dccdc9dabf6bfa57a587b78b6d0.pdf
2020-01-01
111
120
10.32598/Immunoregulation.1.4.229
MicroRNA
Neuroinflammation
Multiple Sclerosis
Experimental autoimmune encephalomyelitis
miR-320
Farideh
Talebi
talebi_f@hotmail.com
1
Department of Medical Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
AUTHOR
Samira
Ghourbani
sgsamsahara@gmail.com
2
Department of Medical Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
AUTHOR
Mohammed
Vojgani
3
Department of Medical Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
AUTHOR
Farshid
Noorbakhsh
f-noorbakhsh@tums.ac.ir
4
Department of Medical Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
LEAD_AUTHOR
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ORIGINAL_ARTICLE
Celecoxib, Angiogenesis, and Wound Healing
Background: Wounds and their healing process are among the most crucial medical issues, especially in the field of dermatology and surgery that imposes notable costs to the health care system. Materials and Methods: Wound healing requires specific fundamental steps, such as angiogenesis and inflammation. Angiogenesis is controlled by different cytokines such as Hypoxia-Inducible Factor α (HIF-α), Vascular Endothelial Growth Factor (VEGF), basic Fibroblast Growth Factor (bFGF), Platelet-Derived Growth Factor (PDGF), Tumor Necrosis Factor α (TNF-α), and Matrix MetalloProteinases (MMPs).Results: Celecoxib, an inhibitor of Cyclooxygenase-2 (COX-2), is widely used in medicine and different fields. This medication can inhibit angiogenesis via suppressing all mentioned cytokines. Thus, suppression of angiogenesis by celecoxib, especially in chronic wounds, may result in the poor or delayed healing. Conclusion: Authors suggest complementary clinical studies to evaluate the possible role of celecoxib on the wound healing focusing on angiogenesis.
https://immunoreg.shahed.ac.ir/article_930_663ab126c608faaddc3941bd0c4c17e5.pdf
2020-01-01
121
124
10.32598/Immunoregulation.1.4.239
Celecoxib
Angiogenesis
Wound healing
Cyclooxygenase-2 (COX-2) inhibitor
Amir
Norooznezhad
norooznezhad@gmail.com
1
Medical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.
LEAD_AUTHOR
Fatemeh
Norooznezhad
fateme.noroznezhad@gmail.com
2
Medical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.
AUTHOR
Ali
Mostafie
ali_mostafaie@yahoo.com
3
Medical Biology Research Center, Health Technology Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.
AUTHOR
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