(955.1) Antibiotics and High-Fat-Diet Induced Gut Inflammation and Impaired Gut Permeability are Improved by Dietary Blueberries Possibly Through NFκB Signaling

Poster Board Number: E578

Ceres Mattos Della Lucia (University of Utah, Federal University of Vicosa), Chrissa Petersen (University of Utah), Satheesh Babu Adhini Kuppuswamy (University of Utah), Anandh Babu Pon Velayutham (University of Utah)

Background:  Evidence indicates that a high fat diet can promote gut inflammation and increase gut permeability. The use of antibiotics further exacerbates these complications and can lead to the development of inflammatory bowel disease. Blueberries are rich in bioactive components such as anthocyanins. We recently reported the vascular and prebiotic effects of dietary blueberries. However, the effects of blueberries on gut inflammation and permeability are unknown. In the present study, we tested the hypothesis that blueberries improve antibiotics and high-fat-diet (HFD) induced gut inflammation and impaired gut barrier function in C57BL/6J mice.

Methods:  7-week-old male mice (Jackson Lab) consumed standard diet (10% kcal fat) (CON) or HFD (60% kcal fat) with antibiotic cocktail (ampicillin, vancomycin, neomycin sulfate and metronidazole) in drinking water (HFA) or 3.7% freeze-dried blueberry powder supplemented HFD with antibiotic cocktail in drinking water (HFA+BB) for 12 weeks. Body weight and body composition were assessed at the end of the experiment. Inflammation and permeability of the colon were assessed by the mRNA expression of inflammatory markers (IL-1β, IL-6, iNOS, MCP-1); gut barrier markers (MUC-2, cldn-1 and TJP-10); and markers of NFκB signaling (p65, IKK- β and IκBα) by qPCR using specific primers and SYBR green.

Results:  HFA mice had an increased body weight, reduced lean body mass, and increased body fat compared to CON mice. Blueberry supplementation did not alter these metabolic parameters in HFA+BB vs HFA mice. mRNA expression of inflammatory markers (IL-1β, iNOS, MCP-1); gut barrier marker MUC-2; and markers of NFκB signaling (p65 and IκBα) were increased in HFA vs CON mice. However, blueberry supplementation improved inflammation and permeability of the colon as shown by a reduced colonic expression of IL-1β, iNOS, MCP-1 and MUC-2 in HFA+BB vs HFA mice. Further, a reduced mRNA expression of p65 and IκBα in HFA+BB vs HFA mice indicates that the protective effect of blueberry on the colon could be mediated through NFκB signaling.

Conclusion:  Blueberry supplementation suppresses colon inflammation and ameliorates colon permeability possibly through NFκB Signaling. Consumption of blueberry is a potential dietary approach to improve gut health.

NIH/NCCIH (R01AT010247) and USDA/NIFA (2018-67018-27510 amp;amp; 2019-67017-2925) to Anandh Babu Pon Velayutham