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. 2018 Feb 15:2018:8430614.
doi: 10.1155/2018/8430614. eCollection 2018.

Dietary n-3 PUFA May Attenuate Experimental Colitis

Cloé Charpentier  1   2 , Ronald Chan  3 , Emmeline Salameh  1 , Khaly Mbodji  1 , Aito Ueno  3   4 , Moïse Coëffier  1   5 , Charlène Guérin  1 , Subrata Ghosh  3   6 , Guillaume Savoye  1   2 , Rachel Marion-Letellier  1
Affiliations

Dietary n-3 PUFA May Attenuate Experimental Colitis

Cloé Charpentier et al. Mediators Inflamm. .

Abstract

Background: Inflammatory bowel diseases (IBD) occurred in genetically predisposed people exposed to environmental triggers. Diet has long been suspected to contribute to the development of IBD. Supplementation with n-3 polyunsaturated fatty acids (PUFA) protects against intestinal inflammation in rodent models while clinical trials showed no benefits. We hypothesized that intervention timing is crucial and dietary fatty acid pattern may influence intestinal environment to modify inflammation genesis. The aim of this study was to evaluate the dietary effect of PUFA composition on intestinal inflammation.

Methods: Animals received diet varying in their PUFA composition for four weeks before TNBS-induced colitis. Colon inflammatory markers and gut barrier function parameters were assessed. Inflammatory pathway PCR arrays were determined.

Results: n-3 diet significantly decreased colon iNOS, COX-2 expression, IL-6 production, and LTB4 production but tended to decrease colon TNFα production (P = 0.0617) compared to control diet. Tight junction protein (claudin-1, occludin) expressions and MUC2 and TFF3 mRNA levels were not different among groups. n-9 diet also decreased colon IL-6 production (P < 0.05).

Conclusions: Dietary n-3 PUFA influence colitis development by attenuating inflammatory markers. Further research is required to better define dietary advice with a scientific rationale.

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Figures

Figure 1
Figure 1
Experimental design and clinical parameters in rats receiving diets varying in their unsaturated fatty acid composition followed by TNBS-induced colitis. (a) Experimental design. Rats received diets varying in their PUFA composition for four weeks before colitis induction at day 0. Rats were killed at day 2. (b) Body weight at day 2. (c) Body weight follow-up from day 28 to day 2. ∗∗ means P < 0.01 versus all colitis groups (TNBS, n-3, n-6, and n-9).
Figure 2
Figure 2
Inflammatory markers in rats receiving diets varying in their unsaturated fatty acid composition for 4 weeks followed by TNBS-induced colitis. (a) Colon/weight length at day 2. (b) Colon iNOS expression with a representative gel at day 2. (c) Colon IL-6 and (d) TNFα production. 5-Aminosalicylic acid (5-ASA) is used a positive anti-inflammatory control. Data from colitic rats were compared by 1-way ANOVA followed by Tukey posttests. ∗∗ means P < 0.01 versus CTRL, ∗∗∗ means P < 0.001 versus CTRL, and ∗ means P < 0.05 versus TNBS.
Figure 3
Figure 3
Eicosanoid pathway in rats varying in their unsaturated fatty acid composition for 4 weeks followed by TNBS-induced colitis. (a) Colon cyclooxygenase-2 (COX-2) expression with a representative gel and (b) colon LTB4 production at day 2. 5-Aminosalicylic acid (5-ASA) is used a positive anti-inflammatory control. Data from colitic rats were compared by 1-way ANOVA followed by Tukey posttests. ∗ means P < 0.05 versus TNBS, ∗∗∗ means P < 0.001 versus TNBS, and $ means P < 0.05 versus n-3.
Figure 4
Figure 4
Gut barrier parameters in rats receiving diets varying in their unsaturated fatty acid composition for 4 weeks followed by TNBS-induced colitis. (a) Colon claudin-1 expression, (b) occludin expression, (c) trefoil factor 3 (TFF3) mRNA level, and (d) MUC2 mRNA level at day 2. (e) Representative gel of colon claudin-1 and occludin expression. 5-Aminosalicylic acid (5-ASA) is used a positive anti-inflammatory control. Data from colitic rats were compared by 1-way ANOVA followed by Tukey posttests.
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