Production of experimental ulcerative colitis in gnotobiotic guinea pigs with simplified microflora

Abstract

Conventional guinea pigs provided with a solution of 5% (wt/vol) degraded carrageenan as the sole source of oral fluids developed ulcerations of their ceca and large intestines within 30 days. Similar lesions were not detected in germfree guinea pigs treated in an identical manner, suggesting that an intestinal microflora was necessary for development of intestinal lesions. To simplify the bacterial flora required for production of cecal ulcerations, 10 pools consisting of 10 bacterial strains each were isolated from the cecal microflora of carrageenan-treated animals. Groups of germfree guinea pigs were associated with 2 of the 10 pools by orogastric intubation and observed for development of disease. One-half of each group was treated with carrageenan. The two bacterial pools were characterized by the presence of cytopathic effects for WI-38 and Vero cells, increased chemotactic activity, and increased concentrations of long-chain fatty acids. The results indicated that animals associated with these two pools developed cecal ulcerations during carrageenan treatment. Preliminary results also indicated that cecal ulcerations developed in germfree animals mono-associated with a strain of Bacteroides vulgatus isolated from one of the pools, regardless of whether carrageenan was administered, suggesting a bacterial involvement in disease development in the absence of carrageenan treatment.

Bacterial-induced Inflammation in Germ-free Rabbit Appendix

“…B. vulgatus was the dominant bacterial stimulus in carrageenan-induced colitis in guinea pigs. 21 The inflammation seen in the HLA-B27 rats treated with microbiota supplemented with B. vulgatus had less inflammation than that seen in specific pathogen-free colonized mice. However, these rats displayed more inflammation than that produced by a subset of bacteria that lacked B. vulgatus, showing that additional bacterial interactions are involved in developing inflammation.…”

Sialylation and fucosylation modulate inflammasome-activating eIF2 Signaling and microbial translocation during HIV infection

“…Bacteroides is a taxonomically diverse genus with several species that are known to produce glycan-degrading enzymes and possibly contribute to the exacerbation of inflammation during IBD. [33][34][35][36][37][38][39][40][41][42][43][44][45][46][47] In order to identify the Bacteroides species that are most abundant in our samples, and thus are potentiality responsible for the aforementioned correlations, we performed an additional analysis on the Amplicon Sequence Variants (ASVs) related to the Bacteroides species. We focused on species that have >1% relative abundance across samples and found in >20% of the samples.…”

“…33,34 Some of these commensal bacterial strains are associated with inflammation during colitis and other inflammatory bowel diseases (IBD) in humans, [35][36][37][38][39][40][41][42][43] and can induce inflammation and colitis in animal models. [44][45][46][47] Furthermore, the ability of B. vulgatus to catabolize sialic acid during colitis induces intestinal inflammation by driving dysbiosis manifested by Enterobacteriaceae expansion. 33 These reports support the notion that elevated sialic acid catabolism by the commensal gut microbiome may have a detrimental influence on the gut microenvironment.…”

Differential effect of immune cells on non‐pathogenic Gram‐negative bacteria‐induced nuclear factor‐κB activation and pro‐inflammatory gene expression in intestinal epithelial cells

“…[7][8][9] In addition, a mechanistic role for the enteric bacterial flora in the pathogenesis of chronic mucosal inflammation is shown in various animal models of experimental colitis. 10,11 For example, reconstitution studies of gnotobiotic HLA-B27 transgenic rats 12,13 and carrageenan-induced colitis in guinea pigs 14 implicate B. vulgatus as particularly important to the induction of colitis in these models. In contrast, Autenrieth and colleagues showed protective effects of B. vulgatus on the development of E. coli-mediated experimental colitis in interleukin (IL)-2 -/mice.…”