Nutrient-induced inflammation in the intestine

Abstract

Purpose of review: To review our current understanding of the relationship between absorption of nutrients and intestinal inflammatory response.

Recent findings: There is increasing evidence linking gut local inflammatory events with the intake of nutrients. Our recent studies, using the conscious lymph fistula rat model, demonstrate that fat absorption activates the intestinal mucosal mast cells. This is accompanied by a dramatic increase in the lymphatic release of mast cell mediators including histamine, rat mucosal mast cell protease II (RMCPII), as well as the lipid mediator prostaglandin D2 (PGD2). Clinical studies suggest that increased consumption of animal fat may play a role in the pathogenesis of inflammatory bowel disease. This impact of dietary fat may not be restricted to the gut but may extend to the whole body. There is evidence linking a high-fat diet-induced metabolic syndrome, with a low-grade chronic inflammatory state. In this review, we hope to convince the readers that fat absorption can have far reaching physiological and pathophysiological consequences.

Summary: Understanding the relationship between nutrient absorption and intestinal inflammation is important. We need a better understanding of the interaction between enterocytes and the intestinal immune cells in nutrient absorption and the gut inflammatory responses.

Figure 1. Basal portion of jejunal absorptive cells and basement membrane from a rat absorbing lipid

Note large intracellular spaces (ISs) between absorptive cells and chylomicrons contained within it. Continuous basement membrane is applied closely to basal plasma membrane of absorptive cells (magnification ×27 600). BM, basement membrane. Used with permission from American Physiological Society.

Figure 2. This electron micrograph demonstrates a break at basement membrane (arrows) and chylomicrons can be seen moving from intercellular space to lamina propria (magnification ×27 600)

IS, intercellular space; LP, lamina propria. Used with permission from American Physiological Society.