Steamed broccoli sprouts alleviate DSS-induced inflammation and retain gut microbial biogeography in mice

Abstract

Inflammatory Bowel Diseases (IBD) are devastating conditions of the gastrointestinal tract with limited treatments, and dietary intervention may be effective, affordable, and safe for managing symptoms. Ongoing research has identified inactive compounds in broccoli sprouts, glucoraphanin, and indicated that mammalian gut microbiota play a role in metabolizing it to the anti-inflammatory sulforaphane. The biogeographic location of participating microbiota and how that affects anti-inflammatory benefits to the host is unknown. We fed specific pathogen free C57BL/6 mice either a control diet or a 10% steamed broccoli sprout diet, and gave a three-cycle regimen of 2.5% dextran sodium sulfate (DSS) in drinking water over a 40-day experiment to simulate chronic, relapsing ulcerative colitis. We monitored body weight, fecal characteristics, fecal lipocalin, and bacterial communities from the digesta and epithelium in the jejunum, cecum, and colon. Mice fed the broccoli sprout diet while receiving DSS performed better than mice fed the control diet while receiving DSS for all disease parameters, including significantly more weight gain, lower Disease Activity Index scores, and higher bacterial richness in all gut locations. Bacterial communities were assorted by gut location except in the mice receiving the control diet and DSS treatment. Importantly, our results suggested that broccoli sprout feeding completely abrogated the effects of DSS on gut microbiota, as bacterial communities were similar between mice receiving broccoli sprouts with and without DSS. Collectively, these results strongly support the protective effect of steamed broccoli sprouts against gut microbiota dysbiosis and development of colitis induced by DSS.

Early life exposure to broccoli sprouts confers stronger protection against enterocolitis development in an immunological mouse model of inflammatory bowel disease

“…Mice have a large cecum, even in IL-10-ko mice this organ acquires a diverse microbiota given enough microbial exposure and time (64). Studies on inflammation for IBD models report significant inflammation and changes to cecal microbiota in mice (21, 90, 91). It is likely that given the short duration of this experimental period, the cecum and parts of the colon that also house diverse microbiota were the only organs which were suited to recruit differential bacterial communities fast enough to be statistically significant.…”

“…Mice have a large cecum, even in IL-10-ko mice this organ acquires a diverse microbiota given enough microbial exposure and time (64). Studies on inflammation for IBD models report significant inflammation and changes to cecal microbiota in mice (21,90,91).…”

“…Specifically, sulforaphane (SFN), the most well-studied isothiocyanate, inhibits the immune factor NF-kB and downregulates multiple inflammatory signaling pathways (9). Broccoli sprouts, or the purified SFN or precursor compounds, protect against chemical-induced ulcerative colitis in mice (20, 21), but the applicability of previous diet research to CD has been hampered by the use of mouse models which lack the complex immune-dysfunction component of CD (22, 23). Medical professionals will need a clear understanding of how the immune system in CD patients will react to the microbiota changes induced by diet (18, 24), and especially the inclusion of a sulfur-rich diet which complicates hot-microbe interactions in the gut (25), as CD patients are historically been advised to avoid cruciferous vegetables (24).…”

Research advancements and perspectives of inflammatory bowel disease: A comprehensive review

“…Many dietary contents have protective potential in IBD treatments, such as Spermidine, Chlorophyllin in green vegetables, steamed or raw broccoli sprouts with high levels of sulforaphane and fruits like avocado. 54 – 59 Spermidine, with high levels in soybeans, wheat germ, and aged cheese, has strong anti-inflammatory potential via promoting an M2-like macrophage differentiation, while it is ineffective in the macrophages of IBD patients carrying PTPN2 SNP rs1893217. 54 Mannose, exerts a potential therapeutic effect on both DSS-induced and IL-10-deficient colitis mouse models by limiting cathepsin B release from lysosomes which prevents mitochondrial dysfunction and TJs disruption.…”