Abstract
Helminths may alter the immunoinflammatory reactions of colitis. Proteins derived from H. polygyrus have prospective therapy for colitis. The goal of this study was to interpret the protective mechanisms of L4 somatic antigen (LSA) from Heligmosomoides polygyrus against an inflammatory response to the pathogenesis of DNBS-induced colitis. Colitis was actuated in mice by rectal instillation of DNBS. The mice were randomly divided into five groups containing control, DNBS alone, and three groups, with different doses of LSA (50, 100, and 200 μg/mL), respectively. Mice initiated colitis by rectal administration of DNBS and after that were immunized with LSA for 14 days. Mice treated with LSA inhibited wasting disease compared with DNBS only group. The percentages of cells producing IFN-γ were reduced by LSA treatment. The level of T lymphocytes CD4+IFN-γ+ cells in the LPL was significantly diminished by LSA at both 100 and 200 μg/mL groups (p<0.05). The mRNA expression of T-bet was significantly declined in LSA immunized mice, but not RORγ-T mRNA, whereas GATA-3 expression tended to increase. The activation of STAT-4 significantly reduced LSA-treated mice but not STAT-1. It can be concluded that T-bet is required for optimal production of IFN-γ in colitis.
Highlights
Ulcerative colitis (UC) is an inflammatory bowel disease that causes long-lasting inflammation in the inner most lining of the colon [1, 2]
We examined whether L4 somatic antigen (LSA) could enhance the dinitrobenzene sulfonic acid (DNBS)-induced acute colitis
We found that LSA injection had a significant inhibitory effect on mRNA T-bet expression and IFNγ percentages
Summary
Ulcerative colitis (UC) is an inflammatory bowel disease that causes long-lasting inflammation in the inner most lining of the colon [1, 2]. UC is a chronic immune disorder affecting the gastrointestinal tract It is a chronic gastrointestinal illness described by inflammatory changes and mucosal tissue damage [3, 4]. Obsessive signs of UC incorporate ulceration of the mucosa, decreasing and loss of the crypts, and infiltration of inflammatory cells [5, 6]. The signs of colitis stimulated by 2,4-dinitrobenzene sulfonic acid (DNBS) in a rodents models are similar to human UC; these incorporate looseness of the bowels, loss of body weight, shortening of the colon, ulceration of the mucosa, and histopathological lesions as in human UC [5,6,7,8,9]. Many researchers described that a treatment including infection with live worms decreases the inflammation related to autoimmune diseases, as Crohn’s disease [8, 10]. Generation of Th1 cells from naive precursors requires T-bet signaling that leads to activation
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