Retinoic acid decreases the severity of Salmonella enterica serovar Typhimurium mediated gastroenteritis in a mouse model

被引:13
作者
Sinha, Ritam [1 ]
Howlader, Debaki Ranjan [1 ]
Mukherjee, Priyadarshini [1 ]
Rai, Sulabh [1 ]
Nag, Dhrubajyoti [1 ]
Koley, Hemanta [1 ]
机构
[1] Natl Inst Cholera & Enter Dis, Div Bacteriol, P-33,CIT Rd, Kolkata 700010, India
关键词
Gastroenteritis; Salmonella enterica serover Typhimurium; All trans retinoic acid; Regulatory T cells; FoxP3; VITAMIN-A; T-CELLS; RESPONSES; RECEPTOR; EXPRESSION; CHILDREN; COLITIS; INFLAMMATION; PATHOGEN; IMPACT;
D O I
10.1016/j.imbio.2016.01.011
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Gastroenteritis is a global burden; it's the major cause of morbidity and mortality both in adults and children of developing countries. Salmonella is one of the leading causes of bacteria-mediated gastroenteritis and due to its increasing multidrug antibiotic resistance; Salmonella-mediated gastroenteritis is difficult to control. Retinoic acid, the biologically active agent of vitamin A has an anti-inflammatory effect on experimental colitis. In this study we have shown All trans retinoic acid (ATRA) treatment down regulates Salmonella-mediated colitis in a murine model. Macroscopic signs of inflammation such as decrease in body weight and cecum weight, shorter length of proximal colon and pathological score of colitis were observed less in ATRA treated mice than in a vehicle control group. ATRA treatment not only reduced pro-inflammatory cytokine responses, such as TNF-alpha, IL-6, IL-1 beta, IFN-gamma and IL-17 production but also increased IL-10 response in the supernatant of intestinal tissue. Results also suggested that ATRA treatment enhances the number of FoxP3-expressing T regulatory cells in MLN and also decreases bacterial load in systemic organs. We concluded that ATRA treatment indeed reduces Salmonella Typhimurium-mediated gastroenteritis in mice, suggesting it could be an important part of an alternative therapeutic approach to combat the disease. (C) 2016 Elsevier GmbH. All rights reserved.
引用
收藏
页码:839 / 844
页数:6
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