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

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.
Applied physiology, nutrition and metabolism 2018 v.43 no.9 pp. 893-901
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
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.