Dietary glutamine increases secretory IgA and may suppress gram‐negative bacterial translocation in a rat model of short bowel syndrome (SBS)

Abstract

Background Normal gut barrier function is dependent upon mucosal gut-associated lymphoid tissue and anatomic factors (e.g. tight junctions). Previous studies in animal models of SBS after massive small bowel resection (SBR) show that increased translocation of luminal bacteria (BT) may occur, signifying abnormal gut barrier function. In this study, we investigated BT, fecal levels of secretory IgA (sIgA) and responses to dietary glutamine (GLN) and oral antibiotic therapy in a rat model of combined small-bowel-colonic resection. Methods Adult Sprague-Dawley rats underwent resection of 60% of distal small bowel and proximal colon (RX) or small bowel transection (TX; control). Rats were pair-fed diets ± L-glutamine (GLN; 4% of diet) for 3 weeks after intestinal surgery. Oral antibiotics [neomycin, metronidazole, and polymyxin; (Abx)] were given in one RX group. At sacrifice, mesentery lymph nodes (MLN) were cultured for gram-negative bacteria as an index of BT. Fecal sIgA was determined on days 1, 6, 13 and 21 by ELISA. Results RX significantly increased bacterial positivity in MLN (1/9 TX rats vs 7/9 RX rats; P<0.02), concomitant with a marked increase in fecal sIgA over time (15-fold increase RX vs TX day 21; P<0.001). Oral Abx eliminated RX-induced BT and decreased fecal sIgA (P<0.02). Dietary GLN after RX markedly increased sIgA (P<0.001 vs all other groups) and blunted BT (2/6; NS). Conclusion RX-induced BT occurs despite an increase in sIgA. Dietary GLN augments the sIgA response, which may play a role in protection against BT in this model. Supported by DK55850.