Bacterial antigens alone can influence intestinal barrier integrity, but live bacteria are required for initiation of intestinal inflammation and injury

Abstract

Intestinal flora plays a critical role in the initiation and perpetuation of inflammatory bowel disease. This study examined whether live fecal bacteria were necessary for the initiation of this inflammatory response or whether sterile fecal material would provoke a similar response. Three preparations of fecal material were prepared: (1) a slurry of live fecal bacteria, (2) a sterile lysate of bacterial antigens, and (3) a sterile filtrate of fecal water. Each preparation was introduced via gastric gavage into the intestines of axenic interleukin-10 gene-deficient mice genetically predisposed to develop inflammatory bowel disease. Intestinal barrier integrity and degrees of mucosal and systemic inflammations were determined for each preparation group. Intestinal barrier integrity, as determined by mannitol transmural flux, was altered by both live fecal bacterial and sterile lysates of bacterial antigens, although it was not altered by sterile filtrates of fecal water. However, only live fecal bacteria initiated mucosal inflammation and injury and a systemic immune response. Fecal bacterial antigens in the presence of live bacteria and sterile fecal bacterial antigens have different effects on the initiation and perpetuation of intestinal inflammation.

Detection of galectin-3 in patients with inflammatory bowel diseases: new serum marker of active forms of IBD?

“…Gut microbiota are assumed to elicit dysregulation in intestinal immune responses and hereby may become a factor in pathogenetic mechanisms of IBD [37][38][39][40][41]. Interestingly, binding sites for labeled bacteria were visualized on leukocytes in the lamina propria of IBD patients.…”

Change of intestinal mucosa barrier function in the progress of non-alcoholic steatohepatitis in rats

“…Intestinal mucosa barriers include mechanical barrier, chemical barrier, immunologic barrier and biology barrier [18][19][20][21] , any damage of these barriers will damage intestinal mucosa barrier function. In this study, we used plasma D-xylose, endotoxin and intestine mucus sIgA to evaluate the intestinal mucosa barrier function in rats with NASH and to observe its change in NASH rats.…”

Epithelial barrier disruption allows nondisease-causing bacteria to initiate and sustain IBD in the IL-10 gene-deficient mouse

“…Furthermore, we have recently demonstrated that bacterial antigens alone are able to affect the epithelial integrity; however, live bacteria are necessary to cause a sustained inflammation. 22 In this experiment we first established a dose at which indomethacin disrupts the intestinal epithelial barrier integrity in the absence of an intestinal or systemic inflammatory response. We then used this dose of indomethacin to investigate the effects of epithelial barrier disruption and increased permeability on IBD-prone axenic mice monoassociated with a single nondisease-causing bacteria.…”