GUT microbiota, dietary fiber, and inflammatory bowel disease

The National Institute of Diabetes and Digestive and Kidney Diseases awarded Georgia State University Research Foundation Inc. $786,149 on July 15, 2026, under the Diabetes, Digestive, and Kidney Diseases Extramural Research program (CFDA 93.847) to investigate the mechanisms by which dietary fiber types affect intestinal inflammation and inflammatory bowel disease through gut microbiota interactions.

The research addresses empirical gaps in understanding whether increased consumption of fiber-enriched foods and purified fiber supplements provides health benefits or carries risks, particularly regarding inflammatory bowel disease and metabolic syndrome. Prior mouse model studies demonstrated that fiber can mitigate or exacerbate intestinal inflammation in fiber-specific ways, yet the underlying mechanisms remain poorly understood, impeding rational development of fiber-enriched foods and supplements as safe and effective therapeutics. This project will help fill that knowledge gap.

The award runs through June 30, 2030, with work performed in Atlanta, Georgia. University of Toledo serves as a sub-recipient under a statement of work executed August 17, 2026. Dr. Matam Vijay-Kumar acts as the University of Toledo site principal investigator and will participate in bimonthly progress meetings with Georgia State University personnel to discuss experimental design, data interpretation, and manuscript development. University of Toledo provides budgeted personnel and facilities support for the award's technical tasks.

The assistance type is a Project Grant.

Abstract

A large body of epidemiological research suggests an important role for dietary fiber, the collective term for the components of plant-based foods that cannot be catabolized by human digestive enzymes, in promoting health more specifically, consumption of fiber-rich diets is associated with reduced risk of developing numerous chronic inflammatory diseases, including diseases that primarily affect the intestinal tract, such as inflammatory bowel diseases (IBD), as well as the wide array of diseases associated with low-grade intestinal inflammation including metabolic syndrome and cancer. These associations have led to the one-size-fits-all recommendation to eat more fiber prompting increased consumption of foods labeled "high-fiber", which, in the U.S., includes foods naturally rich in fiber such as whole wheat breads and highly processed foods (HPF) enriched with refined fibers such as inulin. Additionally, consumption of purified fiber supplements, the most common of which is psyllium, has increased. However, the extent to which such increased fiber consumption is beneficial, or even safe, is far from clear. Some interventional studies reported marked benefits while others observed minimal effects and individual case reports suggest the possibility of rare but devastating consequences. Our studies in tractable mouse models demonstrate that enriching diets with fiber can, in a fiber-specific manner, mitigate or exacerbate intestinal inflammation via mechanisms that remain poorly understood. Such ignorance impedes rational development of fiber-enriched foods and fiber supplements as safe and effective health tools. The central goal of this proposal is to help fill this GAP in critical knowledge. The current paradigm treats fiber supplements as a monolithic entity or in binary format as insoluble or soluble chemicals with the former providing motility-promoting bulk while the latter is metabolized by microbiota to short-chain fatty acids (scfa), which have an array of beneficial impacts. Our work challenges that paradigm, which is too rudimentary and fails to capture the breadth of fiber's impacts on the intestine. Rather, we find that distinct purified fibers have diverse bioactions, many of which are mediated by microbiota but not by scfa. Furthermore, the mechanisms of action of the mixtures of fibers naturally present in food, and thus more likely to reflect benefits of foods naturally rich in fiber have barely been studied. We propose to fill these foundational knowledge gaps focusing on specific questions germane to rational, safe, and effective deployment of fiber supplements and fiber- enriched foods. We use murine colitis models as a tractable platform of mechanistic discovery but anticipate results that our results will be applicable to other inflammatory diseases and testable in humans.