(OR22-07-23) Kale Vegetable Attenuates Colitis by Abating the Proliferation of Lipopolysaccharide-Producing Gut Bacteria and Augmenting Gut Barrier Integrity

Objectives: Inflammatory Bowel Disease, results from loss of gut integrity, gut dysbiosis and dysregulated immune response. In a previous study we have shown that Kale (Brassica oleracea var. acephala), a functional food rich in bioactive phytochemicals and fiber prevents high-fat (HF) diet-induced inflammation and promotes the growth of beneficial gut bacteria taxa. Herein, we sought to evaluate the protective role of dietary kale against acute inflammation. We hypothesized that kale supplementation is protective against the severity of dextran sulfate sodium (DSS) induced inflammation by changing the gut microbiota composition and strengthening the gut protective barrier

Methods: Twelve-week-old C57BL6J mice were fed a HF diet with or without 4.5% kale for 2 weeks. Severe colitis was induced by providing 3% DSS (w/v) via drinking water over 7 days during which the disease activity index (DAI) was measured. After euthanasia, macroscopic colon morphology was examined, and the gut microbiota was profiled by 16S rRNA sequencing of colon contents. The gene expression of inflammatory markers and tight junction proteins in colon tissue were determined by RT-PCR.

Results: Kale supplementation attenuated the DAI score, colon shortening, and granuloma formation induced by DSS. Markers of inflammation i.e.,1L-1b, IL-6, TNF-a, iNOS, F4/80, and TLR-4 were downregulated and the gene expression of claudin was upregulated (P < 0.05, n=3). Dietary kale lowered serum levels of LPS binding protein (LBP) (P < 0.05; n=7). Increased LBP corresponds to LPS endotoxemia levels due to a leaky gut. The proliferation of LPS-producing gut bacteria from the family Enterobacteriaceae specifically the genus Enterobacter, genus Klebsiella, Escherichia coli and the family Muribaculaceae were significantly reduced (P < 0.05, n=7) in groups supplemented with kale.

Conclusions: Dietary kale is protective against DSS induced acute gut inflammation through attenuation of LPS production by reducing the proliferation of gut bacteria that produce it. It further enhances expression of Claudin to augment the integrity of the gut barrier.

Funding Sources: New laboratory startup funds awarded to Dr. Diana Obanda by the University of Maryland, College Park, MD.