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Chickpea supplementation prior to colitis onset reduces inflammation in dextran sodium sulfate-treated C57Bl/6 male mice

Author:
Monk, Jennifer M., Wu, Wenqing, McGillis, Laurel H., Wellings, Hannah R., Hutchinson, Amber L., Liddle, Danyelle M., Graf, Daniela, Robinson, Lindsay E., Power, Krista A.
Source:
Applied physiology, nutrition and metabolism 2018 v.43 no.9 pp. 893-901
ISSN:
1715-5320
Subject:
biomarkers, blood serum, chickpeas, colitis, colon, dextran, diet, drinking water, epithelium, flour, gene expression, histology, immunoglobulin A, inflammation, interleukin-10, males, mice, phenolic compounds, protein synthesis, signs and symptoms (animals and humans), sodium, transcription factor NF-kappa B, tumor necrosis factor-alpha
Abstract:
The potential for a chickpea-supplemented diet (rich in fermentable nondigestible carbohydrates and phenolic compounds) to modify the colonic microenvironment and attenuate the severity of acute colonic inflammation was investigated. C57Bl/6 male mice were fed a control basal diet or basal diet supplemented with 20% cooked chickpea flour for 3 weeks prior to acute colitis onset induced by 7-day exposure to dextran sodium sulfate (DSS; 2% w/v in drinking water) and colon and serum levels of inflammatory mediators were assessed. Despite an equal degree of DSS-induced epithelial barrier histological damage and clinical symptoms between dietary groups, biomarkers of the ensuing inflammatory response were attenuated by chickpea pre-feeding, including reduced colon tissue activation of nuclear factor kappa B and inflammatory cytokine production (tumor necrosis factor alpha and interleukin (IL)-18). Additionally, colon protein expression of anti-inflammatory (IL-10) and epithelial repair (IL-22 and IL-27) cytokines were increased by chickpea pre-feeding. Furthermore, during acute colitis, chickpea pre-feeding increased markers of enhanced colonic function, including RelmĪ² and IgA gene expression. Collectively, chickpea pre-feeding modulated the baseline function of the colonic microenvironment, whereby upon induction of acute colitis, the severity of the inflammatory response was attenuated.
Agid:
6439262