T lymphocytes in host defense against bacterial translocation from the gastrointestinal tract

Abstract

Flow cytofluorometric analyses of lymphocytes harvested from the mesenteric lymph node (MLN), mucosal epithelium, and lamina propria of C57BL/6 mice demonstrate that expression of a/Il or y/6 T-cell receptors (TCR) and CD4 or CD8 molecules by T lymphocytes in the intestinal immune system varies depending upon their anatomic location. The MLN contained equivalent numbers of CD4+ and CD8+ T cells, the vast majority of which were a/I TCR positive (a/Il TCR+). The lamina propria T cells were predominantly CD4+ and a/8l TCR+, while the intestinal intraepithelial lymphocytes consisted of equivalent numbers of a/Il and y/ T cells, the majority of which were CD8+. There were no significant changes in these T-cell phenotypic profiles when the mice were antibiotic decontaminated or monoassociated with Escherichia coli. Mice were depleted of CD4+ T cells and/or CD8+ T cells in vivo by intraperitoneal injections of monoclonal antibody GK 1.5 (rat anti-mouse CD4) and/or monoclonal antibody 2.43 (rat anti-mouse CD8). T-cell depletion was confirmed in the MLN, lamina propria, and the intestinal epithelium by flow cytometry. E. coli C25 translocation from the gastrointestinal (GI) tract to the MLN was significantly increased in mice depleted of CD4+ T cells, CD8+ T cells, or both. T-cell-deficient athymic beige/nude mice also exhibited greater levels of E. coli C25 translocation to the MLN than beige/het euthymic littermates. SalmoneUa typhimurium translocation also was increased following CD4+ and CD8+ T-cell depletion in mice monoassociated with S. typhimurium. Depletion of CD4+ and/or CD8+ T cells also increased the translocation to the MLN of certain indigenous GI flora bacteria. These results confirm that T-cell-mediated immunity is involved in the host defense against bacterial translocation from the GI tract.

Role for FimH in Extraintestinal Pathogenic Escherichia coli Invasion and Translocation through the Intestinal Epithelium

“…The process by which bacteria and their products migrate from the GIT to the bloodstream and other organs is called "bacterial translocation," which was first described as a clinical phenomenon by Wolochow and colleagues in the 1960s (1) and was investigated experimentally by Berg and coworkers in the 1980s (2)(3)(4)(5)(6)(7)(8)(9)(10). The latter set of studies defined several risk factors that contribute to translocation, including disruption of gut microflora by antibiotics (4,6), damage or increased permeability of the intestinal epithelial barrier (4,9,11,12), and the health status of the host (4,5,7,8,(10)(11)(12)). In addition, several studies have established an association between the intestinal microflora and systemic infections in immunocompromised individuals (13)(14)(15)(16)(17)(18).…”

Composition and diversity of intestinal coliform flora influence bacterial translocation in rats after hemorrhagic stress

“…Translocation of enteric bacteria depends on disturbance of the intestinal microecology with subsequent bacterial overgrowth (7,10,11,36), impaired host immunity (4,6,20), or physical disruption of the gut mucosal barrier (29,32). Accumulating evidence from human and animal studies suggests that factors such as trauma (18,34) endotoxemia (13,15), hemorrhage (1,2,26), and thermal injury (12,14,30) promote bacterial translocation.…”

Bacterial Translocation

“…Moreover, T-cell depletion not only caused accumulation of bacteria in MLN in healthy rats but also increased bacterial numbers observed in MLN of alcohol-and burn-injured rats and did cause spreading of bacteria to extraintestinal sites (55). Therefore, it appears that appropriate activation of intestinal T cells is critical in maintaining immunity against the translocation of enteric bacteria (108). Additional studies showed the ability of adoptively transferred T cells to confer protection against a number of bacterial infections including E. coli (109).…”