miR-155 deficiency protects mice from experimental colitis by reducing T helper type 1/type 17 responses |
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| حيدر أحمد شمران |
| Authors : Singh, U.P; Murphy, A.E.; Enos, R.T; Shamran, H.A.; Singh, N.P; Guan, H.; Hegde, V.L.; Fan, D.; Price, R.L.; Taub, D.D.; Mishra, M.K.; .; Nagarkatti, M and Nagarkatti, P.S.(2014). |
Summary
Inflammatory bowel disease (IBD), a chronic intestinal inflammatory condition
that affects millions of people worldwide, results in high morbidity
and exorbitant health-care costs. The critical features of both innate and
adaptive immunity are to control inflammation and dysfunction in this
equilibrium is believed to be the reason for the development of IBD.
miR-155, a microRNA, is up-regulated in various inflammatory disease
states, including IBD, and is a positive regulator of T-cell responses. To
date, no reports have defined a function for miR-155 with regard to cellular
responses in IBD. Using an acute experimental colitis model, we found
that miR-155
/
mice, as compared to wild-type control mice, have
decreased clinical scores, a reversal of colitis-associated pathogenesis, and
reduced systemic and mucosal inflammatory cytokines. The increased frequency
of CD4+ lymphocytes in the spleen and lamina propria with dextran
sodium sulphate induction was decreased in miR-155
/
mice.
Similarly, miR-155 deficiency abrogated the increased numbers of interferon-
c expressing CD4+ T cells typically observed in wild-type mice in
this model. The frequency of systemic and mucosal T helper type
17-, CCR9-expressing CD4+ T cells was also reduced in miR-155
/
mice
compared with control mice. These findings strongly support a role for
miR-155 in facilitating pro-inflammatory cellular responses in this model
of IBD. Loss of miR-155 also results in decreases in T helper type 1/type
17, CD11b+, and CD11c+ cells, which correlated with reduced clinical
scores and severity of disease. miR-155 may serve as a potential therapeutic
target for the treatment of IBD.
Keywords: Crohn’s disease; inflammatory bowel disease; miR-155
/
; T
helper type 1/type 17; ulcerative colitis.
Introduction
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2014-9-1
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