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Plos One : Colonic Inflammation in Mice is Improved by Cigarette Smoke Through Inkt Cells Recruitment, Volume 8

By Nguyen, Hang, Thi Thu

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Book Id: WPLBN0003945529
Format Type: PDF eBook :
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Reproduction Date: 2015

Title: Plos One : Colonic Inflammation in Mice is Improved by Cigarette Smoke Through Inkt Cells Recruitment, Volume 8  
Author: Nguyen, Hang, Thi Thu
Volume: Volume 8
Language: English
Subject: Journals, Science, Medical Science
Collections: Periodicals: Journal and Magazine Collection
Publication Date:
Publisher: Plos


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Thu Nguyen, H. T. (n.d.). Plos One : Colonic Inflammation in Mice is Improved by Cigarette Smoke Through Inkt Cells Recruitment, Volume 8. Retrieved from

Description : Cigarette smoke (CS) protects against intestinal inflammation during ulcerative colitis. Immunoregulatory mechanisms sustaining this effect remain unknown. The aim of this study was to assess the effects of CS on experimental colitis and to characterize the intestinal inflammatory response at the cellular and molecular levels. Using the InExposeH System, a smoking device accurately reproducing human smoking habit, we pre-exposed C57BL/6 mice for 2 weeks to CS, and then we induced colitis by administration of dextran sodium sulfate (DSS). This system allowed us to demonstrate that CS exposure improved colonic inflammation (significant decrease in clinical score, body weight loss and weight/length colonic ratio). This improvement was associated with a significant decrease in colonic proinflammatory Th1/Th17 cytokine expression, as compared to unexposed mice (TNF (p = 0.0169), IFNc (p,0.0001), and IL-17 (p = 0.0008)). Smoke exposure also induced an increased expression of IL-10 mRNA (p = 0.0035) and a marked recruitment of iNKT (invariant Natural Killer T: CD45+ TCRb+ CD1d tetramer+) cells in the colon of DSS-untreated mice. Demonstration of the role of iNKT cells in CS-dependent colitis improvement was performed using two different strains of NKT cells deficient mice. Indeed, in Ja18KO and CD1dKO animals, CS exposure failed to induce significant regulation of DSS-induced colitis both at the clinical and molecular levels. Thus, our study demonstrates that iNKT cells are pivotal actors in the CS-dependent protection of the colon. These results highlight the role of intestinal iNKT lymphocytes and their responsiveness to environmental stimuli. Targeting iNKT cells would represent a new therapeutic way for inflammatory bowel diseases.


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