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. 2017 Nov;32(11):1551-1559.
doi: 10.1007/s00384-017-2882-9. Epub 2017 Aug 16.

Protective Effect of Cigarette Smoke on the Course of Dextran Sulfate Sodium-Induced Colitis Is Accompanied by Lymphocyte Subpopulation Changes in the Blood and Colon

Free PMC article

Protective Effect of Cigarette Smoke on the Course of Dextran Sulfate Sodium-Induced Colitis Is Accompanied by Lymphocyte Subpopulation Changes in the Blood and Colon

Jaroslaw Daniluk et al. Int J Colorectal Dis. .
Free PMC article


Background: Cigarette smoke (CS) exerts protective effect against ulcerative colitis. The mechanism of this phenomenon remains unknown. One of the possible explanation by which CS exerts its anti-inflammatory action is modulation of immune system. Therefore, the aim of the study was to evaluate the effect of CS on the course of inflammation and subpopulations of lymphocytes in the blood and colon in mice with dextran sulfate sodium (DSS)-induced colitis.

Methods: C57BL6/cmdb mice were exposed to CS for 4 weeks. Colitis was induced with 3.5% DSS given for 10 days. Severity of colitis was determined by disease activity index (DAI), body weight changes, and macro- and microscopic characteristics of inflammation. Peripheral subpopulations of lymphocytes were assessed by flow cytometry (blood) or immunohistochemistry (colonic tissue).

Results: Mice treated with 3.5% DSS developed severe colitis with significantly decreased body weight, increased DAI, and macroscopic and histological features of colonic inflammation. These findings were diminished after concomitant exposure to CS. Mice exposed to DSS alone demonstrated significantly decreased percentage of total CD4+ cells (73.1 vs. 52%, p = 0.0007), accompanied by increase of CD8+ cells (18.4 vs. 39.5%, p = 0.0001). Concomitant CS exposure reversed inappropriate CD4+/CD8+ ratio both in the blood and colon and significantly increased B cell presence in the colon.

Conclusions: Our study has demonstrated that CS exposure decreases severity of DSS-induced colitis. This phenomenon was accompanied by changes in CD4/CD8 ratio and B cell level in the peripheral blood and colon. These mechanisms may be responsible for protective effect of smoking in ulcerative colitis.

Keywords: Cigarette smoking; Immune response; Inflammatory bowel disease; Ulcerative colitis.

Conflict of interest statement

Conflicts of interest

The authors declare that they have no conflicts of interest.


Fig. 1
Fig. 1
Colonic histopathological features of DSS-induced colitis. Representative H&E staining of colon sections of control mice (a) and mice treated with CS (b), DSS (c), and CS + DSS (d) (a, d 100×, b 200×, c 400×). 3.5% DSS caused severe mucosal damage and infiltration by polymorphonuclear cells and lymphocytes (c). Concomitant exposure to cigarette smoke ameliorated the severity of inflammation (d)
Fig. 2
Fig. 2
Effect of CS, DSS, and CS + DSS exposure on blood lymphocyte subsets. The percentage of T cells (a), B cells (b), total CD 4+ cells (c), and CD8+ cells (d) was determined in the blood of mice by flow cytometry (n = 10 mice/group). CS cigarette smoke, DSS dextran sulfate sodium
Fig. 3
Fig. 3
The effect of cigarette smoke (CS) and dextran sulfate sodium (DSS) on tissue infiltration by lymphocyte subsets. Immunohistochemical staining of mice colonic tissue in DSS-induced colitis with (CS + DSS) or without (DSS) concomitant cigarette smoke exposure. a, b CD4+ cells (magnification a ×400, b ×200). c, d CD8+ cells (magnification c ×200, d ×100). e, f CD20+ cells (magnification e, f ×200)

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