Login Register Cart 0
Generic placeholder image

Current Pharmaceutical Design

Editor-in-Chief

ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Back
Journal Home About Journal Editorial Board Journal Insight Current Issue Volumes/Issues
Subscribe
Review Article

Current Trends in the Treatment of Systemic Lupus Erythematosus

Author(s): Tharsius W. Raja, Duraipandiyan Veeramuthu*, Ignacimuthu Savarimuthu and Naif A. Al-Dhabi

Volume 26, Issue 22, 2020

Page: [2602 - 2609] Pages: 8

DOI: 10.2174/1381612826666200211122633

Price: $65

Abstract

Background: Systemic lupus erythematosus (SLE) is an autoimmune disease in mankind. SLE's downregulation of T and B lymphocytes could cause the development of autoantibodies, which in turn attack cell surface, nuclear, and cytoplasmic molecules, creating immune complexes that harm tissues.

Objective: The objective of the present review is to evaluate SLE's present therapeutic policies and raise consciousness about the disease.

Methods: New therapies are rare for SLE. This is due to the complexity of the disease and its various manifestations. Three techniques are used to develop biological treatments for the illness: B-cell modulation, T-cell regulation and cytokine inhibition. This paper reviews the present trends in SLE therapy.

Results: Each arm of the immune system is a prospective therapeutic development target for this disease; it involves B-cells, T-cells, interferon (IFN) and cytokines. To date, only one of these agents is been approved for use against lupus, belimumab which comes under B-cell therapy. Both the innate and the adaptive immune systems are the objectives. Currently, although there is no full SLE remedy, drug therapy can minimize organ injury and control active disease, which relies on immunosuppressants and glucocorticoids.

Conclusion: It is possible to access SLE treatment in the form of T-cell, B-cell and anticytokine therapies. In these therapies, antibodies and antigens interactions play a major part. Another medication for treating SLE is the non-steroidal anti-inflammatory drug such as hydroxychloroquine. Glucocorticoids (GCs) are another antiinflammatory treatment that suppresses the growth of cytokines related to inflammation and prevents the recruitment of leukocyte by reducing endothelial cell permeability.

Keywords: Systemic lupus erythematosus, T cells, B cells, glucocorticoids, interferon, cytokine.

« Previous Next »
[1]
Zhang Y-Z, Li Y-Y. Inflammatory bowel disease: pathogenesis. World J Gastroenterol 2014; 20(1): 91-9.
[http://dx.doi.org/10.3748/wjg.v20.i1.91] [PMID: 24415861]
[2]
Arseneau KO, Tamagawa H, Pizarro TT, Cominelli F. Innate and adaptive immune responses related to IBD pathogenesis. Curr Gastroenterol Rep 2007; 9(6): 508-12.
[http://dx.doi.org/10.1007/s11894-007-0067-3] [PMID: 18377804]
[3]
Hugot J-P. Genetic origin of IBD Inflammatory bowel diseases 2004; 10(suppl_1): S11-5
[http://dx.doi.org/10.1097/00054725-200402001-00003]
[4]
Danese S, Fiocchi C. Etiopathogenesis of inflammatory bowel diseases. World J Gastroenterol 2006; 12(30): 4807-12.
[http://dx.doi.org/10.3748/wjg.v12.i30.4807] [PMID: 16937461]
[5]
Mylonaki M, Langmead L, Pantes A, Johnson F, Rampton DS. Enteric infection in relapse of inflammatory bowel disease: importance of microbiological examination of stool. Eur J Gastroenterol Hepatol 2004; 16(8): 775-8.
[http://dx.doi.org/10.1097/01.meg.0000131040.38607.09] [PMID: 15256979]
[6]
Sasaki M, Klapproth J-MA. The role of bacteria in the pathogenesis of ulcerative colitis. J Signal Transduction 2012; 2012
[http://dx.doi.org/10.1155/2012/704953]
[7]
Ravikumara M, Hinsberger A, Spray CH. Role of methotrexate in the management of Crohn disease. J Pediatr Gastroenterol Nutr 2007; 44(4): 427-30.
[http://dx.doi.org/10.1097/MPG.0b013e3180320689] [PMID: 17414138]
[8]
Maeda M, Watanabe N, Neda H, et al. Serum tumor necrosis factor activity in inflammatory bowel disease. Immunopharmacol Immunotoxicol 1992; 14(3): 451-61.
[http://dx.doi.org/10.3109/08923979209005404] [PMID: 1517530]
[9]
Breese EJ, Michie CA, Nicholls SW, et al. Tumor necrosis factor α-producing cells in the intestinal mucosa of children with inflammatory bowel disease. Gastroenterology 1994; 106(6): 1455-66.
[http://dx.doi.org/10.1016/0016-5085(94)90398-0] [PMID: 8194690]
[10]
van Dullemen HM, van Deventer SJ, Hommes DW, et al. Treatment of Crohn’s disease with anti-tumor necrosis factor chimeric monoclonal antibody (cA2). Gastroenterology 1995; 109(1): 129-35.
[http://dx.doi.org/10.1016/0016-5085(95)90277-5] [PMID: 7797011]
[11]
Kontoyiannis D, Pasparakis M, Pizarro TT, Cominelli F, Kollias G. Impaired on/off regulation of TNF biosynthesis in mice lacking TNF AU-rich elements: implications for joint and gut-associated immunopathologies. Immunity 1999; 10(3): 387-98.
[http://dx.doi.org/10.1016/S1074-7613(00)80038-2] [PMID: 10204494]
[12]
Hanauer SB, Sandborn WJ, Rutgeerts P, et al. Human anti-tumor necrosis factor monoclonal antibody (adalimumab) in Crohn’s disease: the CLASSIC-I trial. Gastroenterology 2006; 130(2): 323-33.
[http://dx.doi.org/10.1053/j.gastro.2005.11.030] [PMID: 16472588]
[13]
Choi J, Kang B, Kim MJ, Sohn I, Lee HJ, Choe YH. Early infliximab yields superior long-term effects on linear growth in pediatric Crohn’s disease patients. Gut Liver 2018; 12(3): 255-62.
[http://dx.doi.org/10.5009/gnl17290] [PMID: 29298460]
[14]
Colombel JF, Sandborn WJ, Rutgeerts P, et al. Adalimumab for maintenance of clinical response and remission in patients with Crohn’s disease: the CHARM trial. Gastroenterology 2007; 132(1): 52-65.
[PMID: 17241859]
[15]
Armuzzi A, Biancone L, Daperno M, et al. Italian Group for the Study of Inflammatory Bowel Disease Adalimumab in active ulcerative colitis: a “real-life” observational study. Dig Liver Dis 2013; 45(9): 738-43.
[http://dx.doi.org/10.1016/j.dld.2013.03.018] [PMID: 23683530]
[16]
Detrez I, Dreesen E, Van Stappen T, et al. Variability in golimumab exposure: a ‘real-life’observational study in active ulcerative colitis. J Crohn’s Colitis 2016; 10(5): 575-81.
[http://dx.doi.org/10.1093/ecco-jcc/jjv241] [PMID: 26738756]
[17]
Sandborn WJ, Feagan BG, Stoinov S, et al. PRECISE 1 Study Investigators Certolizumab pegol for the treatment of Crohn’s disease. N Engl J Med 2007; 357(3): 228-38.
[http://dx.doi.org/10.1056/NEJMoa067594] [PMID: 17634458]
[18]
Schreiber S, Khaliq-Kareemi M, Lawrance IC, et al. PRECISE 2 Study Investigators Maintenance therapy with certolizumab pegol for Crohn’s disease. N Engl J Med 2007; 357(3): 239-50.
[http://dx.doi.org/10.1056/NEJMoa062897] [PMID: 17634459]
[19]
Sandborn WJ, Hanauer SB, Katz S, et al. Etanercept for active Crohn’s disease: a randomized, double-blind, placebo-controlled trial. Gastroenterology 2001; 121(5): 1088-94.
[http://dx.doi.org/10.1053/gast.2001.28674] [PMID: 11677200]
[20]
Van den Brande JM, Braat H, van den Brink GR, et al. Infliximab but not etanercept induces apoptosis in lamina propria T-lymphocytes from patients with Crohn’s disease. Gastroenterology 2003; 124(7): 1774-85.
[http://dx.doi.org/10.1016/S0016-5085(03)00382-2] [PMID: 12806611]
[21]
Sands BE, Anderson FH, Bernstein CN, et al. Infliximab maintenance therapy for fistulizing Crohn’s disease. N Engl J Med 2004; 350(9): 876-85.
[PMID: 14985485]
[22]
Sebastian S, Neilaj S. Practical guidance for the management of inflammatory bowel disease in patients with cancer. Which treatment? Therap Adv Gastroenterol 2019; 12 1756284818817293
[PMID: 30643542]
[23]
Targan SR, Feagan BG, Fedorak RN, et al. International Efficacy of Natalizumab in Crohn’s Disease Response and Remission (ENCORE) Trial Group Natalizumab for the treatment of active Crohn’s disease: results of the ENCORE Trial. Gastroenterology 2007; 132(5): 1672-83.
[http://dx.doi.org/10.1053/j.gastro.2007.03.024] [PMID: 17484865]
[24]
MacDonald JK, McDonald JW. Natalizumab for induction of remission in Crohn’s disease. Cochrane Database of Systematic Reviews 2007; 1 CD006097
[http://dx.doi.org/10.1002/14651858.CD006097.pub2]
[25]
Kleinschmidt-DeMasters BK, Tyler KL. Progressive multifocal leukoencephalopathy complicating treatment with natalizumab and interferon beta-1a for multiple sclerosis. N Engl J Med 2005; 353(4): 369-74.
[http://dx.doi.org/10.1056/NEJMoa051782] [PMID: 15947079]
[26]
Langer-Gould A, Atlas SW, Green AJ, Bollen AW, Pelletier D. Progressive multifocal leukoencephalopathy in a patient treated with natalizumab. N Engl J Med 2005; 353(4): 375-81.
[http://dx.doi.org/10.1056/NEJMoa051847] [PMID: 15947078]
[27]
Van Assche G, Van Ranst M, Sciot R, et al. Progressive multifocal leukoencephalopathy after natalizumab therapy for Crohn’s disease. N Engl J Med 2005; 353(4): 362-8.
[http://dx.doi.org/10.1056/NEJMoa051586] [PMID: 15947080]
[28]
Yousry TA, Major EO, Ryschkewitsch C, et al. Evaluation of patients treated with natalizumab for progressive multifocal leukoencephalopathy. N Engl J Med 2006; 354(9): 924-33.
[PMID: 16510746]
[29]
Zundler S, Schillinger D, Fischer A, et al. Blockade of αEβ7 integrin suppresses accumulation of CD8+ and Th9 lymphocytes from patients with IBD in the inflamed gut in vivo. Gut 2017; 66(11): 1936-48.
[http://dx.doi.org/10.1136/gutjnl-2016-312439] [PMID: 27543429]
[30]
Lamb CA, Mansfield JC, Tew GW, et al. αEβ7 integrin identifies subsets of pro-inflammatory colonic CD4+ T lymphocytes in ulcerative colitis. J Crohn’s Colitis 2017; 11(5): 610-20.
[PMID: 28453768]
[31]
Vermeire S, O’Byrne S, Keir M, et al. Etrolizumab as induction therapy for ulcerative colitis: a randomised, controlled, phase 2 trial. Lancet 2014; 384(9940): 309-18.
[http://dx.doi.org/10.1016/S0140-6736(14)60661-9] [PMID: 24814090]
[32]
Tang MT, Keir ME, Erickson R, et al. Review article: nonclinical and clinical pharmacology, pharmacokinetics and pharmacodynamics of etrolizumab, an anti-β7 integrin therapy for inflammatory bowel disease. Aliment Pharmacol Ther 2018; 47(11): 1440-52.
[http://dx.doi.org/10.1111/apt.14631] [PMID: 29601644]
[33]
Arihiro S, Ohtani H, Suzuki M, et al. Differential expression of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) in ulcerative colitis and Crohn’s disease. Pathol Int 2002; 52(5-6): 367-74.
[http://dx.doi.org/10.1046/j.1440-1827.2002.01365.x] [PMID: 12100519]
[34]
Vermeire S, Sandborn WJ, Danese S, et al. Anti-MAdCAM antibody (PF-00547659) for ulcerative colitis (TURANDOT): a phase 2, randomised, double-blind, placebo-controlled trial. Lancet 2017; 390(10090): 135-44.
[http://dx.doi.org/10.1016/S0140-6736(17)30930-3] [PMID: 28527704]
[35]
Sandborn WJ, Lee SD, Tarabar D, et al. Phase II evaluation of anti-MAdCAM antibody PF-00547659 in the treatment of Crohn’s disease: report of the OPERA study. Gut 2018; 67(10): 1824-35.
[http://dx.doi.org/10.1136/gutjnl-2016-313457] [PMID: 28982740]
[36]
Matloubian M, Lo CG, Cinamon G, et al. Lymphocyte egress from thymus and peripheral lymphoid organs is dependent on S1P receptor 1. Nature 2004; 427(6972): 355-60.
[http://dx.doi.org/10.1038/nature02284] [PMID: 14737169]
[37]
Kappos L, Radue EW, O’Connor P, et al. FREEDOMS Study Group A placebo-controlled trial of oral fingolimod in relapsing multiple sclerosis. N Engl J Med 2010; 362(5): 387-401.
[http://dx.doi.org/10.1056/NEJMoa0909494] [PMID: 20089952]
[38]
Sandborn WJ, Feagan BG, Wolf DC, et al. TOUCHSTONE Study Group Ozanimod induction and maintenance treatment for ulcerative colitis. N Engl J Med 2016; 374(18): 1754-62.
[http://dx.doi.org/10.1056/NEJMoa1513248] [PMID: 27144850]
[39]
Yen D, Cheung J, Scheerens H, et al. IL-23 is essential for T cell-mediated colitis and promotes inflammation via IL-17 and IL-6. J Clin Invest 2006; 116(5): 1310-6.
[http://dx.doi.org/10.1172/JCI21404] [PMID: 16670770]
[40]
Becker C, Dornhoff H, Neufert C, et al. Cutting edge: IL-23 cross-regulates IL-12 production in T cell-dependent experimental colitis. J Immunol 2006; 177(5): 2760-4.
[http://dx.doi.org/10.4049/jimmunol.177.5.2760] [PMID: 16920909]
[41]
Oppmann B, Lesley R, Blom B, et al. Novel p19 protein engages IL-12p40 to form a cytokine, IL-23, with biological activities similar as well as distinct from IL-12. Immunity 2000; 13(5): 715-25.
[http://dx.doi.org/10.1016/S1074-7613(00)00070-4] [PMID: 11114383]
[42]
Moschen AR, Tilg H, Raine T. IL-12, IL-23 and IL-17 in IBD: immunobiology and therapeutic targeting. Nat Rev Gastroenterol Hepatol 2019; 16(3): 185-96.
[http://dx.doi.org/10.1038/s41575-018-0084-8] [PMID: 30478416]
[43]
Oliver J, Rueda B, López-Nevot MA, Gómez-García M, Martín J. Replication of an association between IL23R gene polymorphism with inflammatory bowel disease. Clinical Gastroenterology and Hepatology 2007; 5(8): 977- 81.e2.
[44]
Markham A. Guselkumab: first global approval. Drugs 2017; 77(13): 1487-92.
[http://dx.doi.org/10.1007/s40265-017-0800-7] [PMID: 28819723]
[45]
Kashani A, Schwartz DA. The expanding role of Anti-IL-12 and/or Anti-IL-23 antibodies in the treatment of inflammatory bowel disease. Gastroenterol Hepatol (N Y) 2019; 15(5): 255-65.
[PMID: 31360139]
[46]
Ghoreschi K, Laurence A, O’Shea JJ. Janus kinases in immune cell signaling. Immunol Rev 2009; 228(1): 273-87.
[http://dx.doi.org/10.1111/j.1600-065X.2008.00754.x] [PMID: 19290934]
[47]
Mavers M, Ruderman EM, Perlman H. Intracellular signal pathways: potential for therapies. Curr Rheumatol Rep 2009; 11(5): 378-85.
[http://dx.doi.org/10.1007/s11926-009-0054-9] [PMID: 19772834]
[48]
Narula N, Rubin DT, Sands BE. Novel therapies in inflammatory bowel disease: an evaluation of the evidence. Am J Gastroenterol Suppl 2016; 3(3): 38.
[http://dx.doi.org/10.1038/ajgsup.2016.19]
[49]
Olivera P, Danese S, Peyrin-Biroulet L. JAK inhibition in inflammatory bowel disease. Expert Rev Clin Immunol 2017; 13(7): 693-703.
[http://dx.doi.org/10.1080/1744666X.2017.1291342] [PMID: 28164724]
[50]
Sandborn WJ, Ghosh S, Panes J, et al. Study A3921063 Investigators Tofacitinib, an oral Janus kinase inhibitor, in active ulcerative colitis. N Engl J Med 2012; 367(7): 616-24.
[http://dx.doi.org/10.1056/NEJMoa1112168] [PMID: 22894574]
[51]
Soendergaard C, Bergenheim FH, Bjerrum JT, Nielsen OH. Targeting JAK-STAT signal transduction in IBD. Pharmacol Ther 2018; 192: 100-11.
[http://dx.doi.org/10.1016/j.pharmthera.2018.07.003] [PMID: 30048708]
[52]
Panés J, Sandborn WJ, Schreiber S, et al. Tofacitinib for induction and maintenance therapy of Crohn’s disease: results of two phase IIb randomised placebo-controlled trials. Gut 2017; 66(6): 1049-59.
[http://dx.doi.org/10.1136/gutjnl-2016-312735] [PMID: 28209624]
[53]
Sandborn WJ, Gosh S, Panes J, et al. A phase 2 study of tofacitinib, an oral Janus kinase inhibitor, in patients with Crohn’s disease Clinical Gastroenterology and Hepatology 2014; 12(9): 1485-93 e2.
[http://dx.doi.org/10.1016/j.cgh.2014.01.029]
[54]
Winthrop KL. The emerging safety profile of JAK inhibitors in rheumatic disease. Nat Rev Rheumatol 2017; 13(4): 234-43.
[http://dx.doi.org/10.1038/nrrheum.2017.23] [PMID: 28250461]
[55]
Cohen S, Curtis JR, DeMasi R, et al. Worldwide, 3-year, post-marketing surveillance experience with tofacitinib in rheumatoid arthritis. Rheumatol Ther 2018; 5(1): 283-91.
[http://dx.doi.org/10.1007/s40744-018-0097-3] [PMID: 29470834]
[56]
Salari-Sharif P, Abdollahi M. Phosphodiesterase 4 inhibitors in inflammatory bowel disease: a comprehensive review. Curr Pharm Des 2010; 16(33): 3661-7.
[http://dx.doi.org/10.2174/138161210794079209] [PMID: 21128899]
[57]
Spadaccini M, D’Alessio S, Peyrin-Biroulet L, Danese S. PDE4 inhibition and inflammatory bowel disease: a novel therapeutic avenue. Int J Mol Sci 2017; 18(6): 1276.
[http://dx.doi.org/10.3390/ijms18061276] [PMID: 28617319]
[58]
Reed M, Crosbie D. Apremilast in the treatment of psoriatic arthritis: a perspective review. Ther Adv Musculoskelet Dis 2017; 9(2): 45-53.
[http://dx.doi.org/10.1177/1759720X16673786] [PMID: 28255338]
[59]
Weigmann B, Popp V, Neurath M, Horan G, Schafer P. P-257 apremilast prevents intestinal inflammation in colitis models via influencing epithelial barrier. Inflamm Bowel Dis 2017; 23: S84.
[60]
Bäumler AJ, Sperandio V. Interactions between the microbiota and pathogenic bacteria in the gut. Nature 2016; 535(7610): 85-93.
[http://dx.doi.org/10.1038/nature18849] [PMID: 27383983]
[61]
Reshef L, Kovacs A, Ofer A, et al. Pouch inflammation is associated with a decrease in specific bacterial taxa. Gastroenterology 2015; 149(3): 718-27.
[http://dx.doi.org/10.1053/j.gastro.2015.05.041] [PMID: 26026389]
[62]
Bajer L, Kverka M, Kostovcik M, et al. Distinct gut microbiota profiles in patients with primary sclerosing cholangitis and ulcerative colitis. World J Gastroenterol 2017; 23(25): 4548-58.
[http://dx.doi.org/10.3748/wjg.v23.i25.4548] [PMID: 28740343]
[63]
Sheehan D, Moran C, Shanahan F. The microbiota in inflammatory bowel disease. J Gastroenterol 2015; 50(5): 495-507.
[http://dx.doi.org/10.1007/s00535-015-1064-1] [PMID: 25808229]
[64]
Lopez-Siles M, Duncan SH, Garcia-Gil LJ, Martinez-Medina M. Faecalibacterium prausnitzii: from microbiology to diagnostics and prognostics. ISME J 2017; 11(4): 841-52.
[http://dx.doi.org/10.1038/ismej.2016.176] [PMID: 28045459]
[65]
Takahashi K, Nishida A, Fujimoto T, et al. Reduced abundance of butyrate-producing bacteria species in the fecal microbial community in Crohn’s disease. Digestion 2016; 93(1): 59-65.
[http://dx.doi.org/10.1159/000441768] [PMID: 26789999]
[66]
Kordy K, Romeo AC, Lee DJ, et al. Combination antibiotics improves disease activity and alters microbial communities in children with ulcerative colitis. J Pediatr Gastroenterol Nutr 2018; 67(3): e60-3.
[http://dx.doi.org/10.1097/MPG.0000000000002034] [PMID: 29762192]
[67]
Ledder O, Turner D. Antibiotics in IBD: still a role in the biological era? Inflamm Bowel Dis 2018; 24(8): 1676-88.
[http://dx.doi.org/10.1093/ibd/izy067] [PMID: 29722812]
[68]
Venegas DP, Boehme M, Lyte JM, et al. Short Chain Fatty Acids (SCFAs)-mediated gut epithelial and immune regulation and its relevance for Inflammatory Bowel Diseases. Front Immunol 2019; 10: 4923-44.
[69]
Ganda Mall J-P, Casado-Bedmar M, Winberg ME, Brummer RJ, Schoultz I, Keita ÅV. A β-glucan-based dietary fiber reduces mast cell-induced hyperpermeability in ileum from patients with Crohn’s disease and control subjects. Inflamm Bowel Dis 2017; 24(1): 166-78.
[http://dx.doi.org/10.1093/ibd/izx002] [PMID: 29272475]
[70]
Ganji-Arjenaki M, Rafieian-Kopaei M. Probiotics are a good choice in remission of inflammatory bowel diseases: A meta analysis and systematic review. J Cell Physiol 2018; 233(3): 2091-103.
[http://dx.doi.org/10.1002/jcp.25911] [PMID: 28294322]
[71]
Scarpato E, Russo M, Staiano A. Probiotics in pediatric gastroenterology: emerging indications: inflammatory bowel diseases. J Clin Gastroenterol 2018; 52(Suppl 1, Proceedings from the 9th Probiotics, Prebiotics and New Foods, Nutraceuticals and Botanicals for Nutrition & Human and Microbiota Health Meeting, held in Rome, Italy from September 10 to 12, 2017): S7-9
[http://dx.doi.org/10.1097/MCG.0000000000001095] [PMID: 30036240]
[72]
Bakken JS, Borody T, Brandt LJ, et al. Fecal Microbiota Transplantation Workgroup Treating Clostridium difficile infection with fecal microbiota transplantation. Clin Gastroenterol Hepatol 2011; 9(12): 1044-9.
[http://dx.doi.org/10.1016/j.cgh.2011.08.014] [PMID: 21871249]
[73]
Allegretti JR, Kassam Z, Fischer M, Kelly C, Chan WW. Risk factors for gastrointestinal symptoms following successful eradication of clostridium difficile by fecal microbiota transplantation (FMT). J Clin Gastroenterol 2019; 53(9): e405-8.
[http://dx.doi.org/10.1097/MCG.0000000000001194] [PMID: 30882536]
[74]
Fang H, Fu L, Wang J. Protocol for fecal microbiota transplantation in inflammatory bowel disease: a systematic review and meta-analysis. BioMed research international 2018; 2018 8941340
[http://dx.doi.org/10.1155/2018/8941340]
[75]
Gazit Z, Pelled G, Sheyn D, et al. Mesenchymal stem cells Principles of regenerative medicine. Elsevier 2019; pp. 205-18.
[http://dx.doi.org/10.1016/B978-0-12-809880-6.00014-X]
[76]
Casali A, Batlle E. Intestinal stem cells in mammals and Drosophila. Cell Stem Cell 2009; 4(2): 124-7.
[http://dx.doi.org/10.1016/j.stem.2009.01.009] [PMID: 19200801]
[77]
Thiagarajah JR, Kamin DS, Acra S, et al. PediCODE Consortium. Advances in evaluation of chronic diarrhea in infants. Gastroenterology 2018; 154(8): 2045-2059. e6.
[http://dx.doi.org/10.1053/j.gastro.2018.03.067] [PMID: 29654747]
[78]
Paschalaki KE, Randi AM. Recent advances in endothelial colony forming cells toward their use in clinical translation. Front Med (Lausanne) 2018; 5: 295.
[http://dx.doi.org/10.3389/fmed.2018.00295] [PMID: 30406106]
[79]
Melief SM, Zwaginga JJ, Fibbe WE, Roelofs H. Adipose tissue-derived multipotent stromal cells have a higher immunomodulatory capacity than their bone marrow-derived counterparts. Stem Cells Transl Med 2013; 2(6): 455-63.
[http://dx.doi.org/10.5966/sctm.2012-0184] [PMID: 23694810]
[80]
Aydin S, Şahin F. Stem Cells Derived from Dental Tissues. Adv Exp Med Biol 2019; 1144: 123-32.
[http://dx.doi.org/10.1007/5584_2018_333]
[81]
Wang M, Liang C, Hu H, et al. Intraperitoneal injection (IP), Intravenous injection (IV) or anal injection (AI)? Best way for mesenchymal stem cells transplantation for colitis. Sci Rep 2016; 6: 30696.
[http://dx.doi.org/10.1038/srep30696] [PMID: 27488951]
[82]
da Costa Gonçalves F, Grings M, Nunes NS, et al. Antioxidant properties of mesenchymal stem cells against oxidative stress in a murine model of colitis. Biotechnol Lett 2017; 39(4): 613-22.
[http://dx.doi.org/10.1007/s10529-016-2272-3] [PMID: 28032203]
[83]
Gonçalves FdaC, Schneider N, Pinto FO, et al. Intravenous vs intraperitoneal mesenchymal stem cells administration: what is the best route for treating experimental colitis? World J Gastroenterol 2014; 20(48): 18228-39.
[http://dx.doi.org/10.3748/wjg.v20.i48.18228] [PMID: 25561790]
[84]
Castelo-Branco MT, Soares ID, Lopes DV, et al. Intraperitoneal but not intravenous cryopreserved mesenchymal stromal cells home to the inflamed colon and ameliorate experimental colitis. PLoS One 2012; 7(3) e33360
[http://dx.doi.org/10.1371/journal.pone.0033360] [PMID: 22432015]
[85]
Duijvestein M, Wildenberg ME, Welling MM, et al. Pretreatment with interferon-γ enhances the therapeutic activity of mesenchymal stromal cells in animal models of colitis. Stem Cells 2011; 29(10): 1549-58.
[http://dx.doi.org/10.1002/stem.698] [PMID: 21898680]
[86]
Volarevic V, Gazdic M, Simovic Markovic B, Jovicic N, Djonov V, Arsenijevic N. Mesenchymal stem cell-derived factors: Immuno-modulatory effects and therapeutic potential. Biofactors 2017; 43(5): 633-44.
[http://dx.doi.org/10.1002/biof.1374] [PMID: 28718997]
[87]
Seril DN, Liao J, Yang GY, Yang CS. Oxidative stress and ulcerative colitis-associated carcinogenesis: studies in humans and animal models. Carcinogenesis 2003; 24(3): 353-62.
[http://dx.doi.org/10.1093/carcin/24.3.353] [PMID: 12663492]
[88]
Bouzid D, et al. Oxidative stress markers in intestinal mucosa of Tunisian inflammatory bowel disease patients Saudi journal of gastroenterology: official journal of the Saudi Gastroenterology Association 2013; 19(3): 131.
[http://dx.doi.org/10.4103/1319-3767.111956]
[89]
Damiani CR, Benetton CA, Stoffel C, et al. Oxidative stress and metabolism in animal model of colitis induced by dextran sulfate sodium. J Gastroenterol Hepatol 2007; 22(11): 1846-51.
[http://dx.doi.org/10.1111/j.1440-1746.2007.04890.x] [PMID: 17489966]
[90]
Nair J, Gansauge F, Beger H. et al. Increased etheno-DNA adducts in affected tissues of patients suffering from Crohn’s disease, ulcerative colitis, and chronic pancreatitis. Antioxidants Redox Signaling 2006; 8(5-6): 1003-10.
[http://dx.doi.org/10.1089/ars.2006.8.1003]
[91]
Gasche C, Chang CL, Rhees J, Goel A, Boland CR. Oxidative stress increases frameshift mutations in human colorectal cancer cells. Cancer Res 2001; 61(20): 7444-8.
[PMID: 11606378]
[92]
Tarmin L, Yin J, Harpaz N, et al. Adenomatous polyposis coli gene mutations in ulcerative colitis-associated dysplasias and cancers versus sporadic colon neoplasms. Cancer Res 1995; 55(10): 2035-8.
[PMID: 7743497]
[93]
Rahimi R, Shams-Ardekani MR, Abdollahi M. A review of the efficacy of traditional Iranian medicine for inflammatory bowel disease. World J Gastroenterol 2010; 16(36): 4504-14.
[http://dx.doi.org/10.3748/wjg.v16.i36.4504] [PMID: 20857519]
[94]
Ng SC, Lam YT, Tsoi KK, Chan FK, Sung JJ, Wu JC. Systematic review: the efficacy of herbal therapy in inflammatory bowel disease. Aliment Pharmacol Ther 2013; 38(8): 854-63.
[http://dx.doi.org/10.1111/apt.12464] [PMID: 23981095]
[95]
Najafzadeh M, Reynolds PD, Baumgartner A, Jerwood D, Anderson D. Chaga mushroom extract inhibits oxidative DNA damage in lymphocytes of patients with inflammatory bowel disease. Biofactors 2007; 31(3-4): 191-200.
[http://dx.doi.org/10.1002/biof.5520310306] [PMID: 18997282]
[96]
Koretz RL, Rotblatt M. Complementary and alternative medicine in gastroenterology: the good, the bad, and the ugly. Clin Gastroenterol Hepatol 2004; 2(11): 957-67.
[http://dx.doi.org/10.1016/S1542-3565(04)00461-6] [PMID: 15551247]
[97]
Langmead L, Rampton DS. Review article: herbal treatment in gastrointestinal and liver disease--benefits and dangers. Aliment Pharmacol Ther 2001; 15(9): 1239-52.
[http://dx.doi.org/10.1046/j.1365-2036.2001.01053.x] [PMID: 11552894]

Rights & Permissions Print Cite
Article Metrics
33
1
1
© 2024 Bentham Science Publishers | Privacy Policy