<i>Lactobacillus rhamnosus</i> GG and <i>Lactobacillus casei</i> Suppress <i>Escherichia coli</i>-Induced Chemokine Expression in Intestinal Epithelial Cells

Abstract

Background: Recently, some strains of lactic acid bacteria (LAB) have been reported to prevent the development of atopic dermatitis and to improve allergic symptoms, especially in young children. However, the mechanisms involved in these effects are not fully understood. Intestinal microbiota play critical roles in the development of host immune development and are recognized and regulated by the host through intestinal epithelial cells (IECs). We thus hypothesized that LAB influence the host immune system through the activation of IECs. To begin testing this hypothesis, chemokine expression in IECs exposed to intestinal bacteria was investigated. Methods: Caco-2 cell monolayers were stimulated with different concentrations of various live or heat-killed intestinal bacteria or bacterial components for up to 3 h. Changes in the gene expressions of various chemokines were measured using quantitative real-time PCR. Results: The expressions of CCL20, CXCL8, CXCL10 and CX3CL1 were strongly induced by nonpathogenic Escherichia coli in a dose-dependent manner and were partially induced by some commensal LAB. In contrast, Lactobacillus rhamnosus GG (LGG) and Lactobacillus casei did not induce these chemokine expressions. In addition, LGG significantly suppressed the expressions of CCL20 and CXCL10 induced by E. coli, peptidoglycan or flagellin when cultured simultaneously. Conclusions:LGG and L. casei markedly suppressed E. coli-induced chemokine expression, presumably through the suppression of the Toll-like receptor-mediated signal transduction pathway, at least in part. The clinical importance of this suppressive effect and the mechanisms involved require further investigation; however, such effects can be used as a marker to identify clinically useful LAB.

Oral Administration of Lactobacillus rhamnosus GG Ameliorates Salmonella Infantis-Induced Inflammation in a Pig Model via Activation of the IL-22BP/IL-22/STAT3 Pathway

“…As expected (Sibartie et al, 2009; Toki et al, 2009), we found that LGG suppressed the production of CCL20 in the jejunum induced by oral infection with S . Infantis, although no changes in CCR6 mRNA expression in the small intestine were observed.…”

“…Oral inoculation with S. enteritidis induces CCL20 production in the spleen of mice (Fahy et al, 2004). LGG was shown to significantly suppress E. coli -induced CCL20 expression in Caco-2 cells (Toki et al, 2009). …”

Anti-Infective Activities of Lactobacillus Strains in the Human Intestinal Microbiota: from Probiotics to Gastrointestinal Anti-Infectious Biotherapeutic Agents

“…L. casei Shirota CFCS decreased Salmonella enterica serovar Enteritidis-induced IL-8 production and, in addition, promoted the expression of cytoprotective heat shock protein (Hsp) 70 in Caco-2 cells (221). L. rhamnosus GG suppressed the expression of CCL20 and CXCL10 triggered in Caco-2 cells by effector molecules, peptidoglycan or flagellin, of enterovirulent E. coli (222). In Caco2BBe cells, in which EHEC infection induces the upregulation of proinflammatory genes, preincubation of the pathogen with L. rhamnosus GG prior to infection reduced the EHEC-induced up- (224).…”

Response of corneal epithelial cells toStaphylococcus aureus

“…Sibratie et al 39 showed that the presence of B. infantis could decrease the induction of CCL20 by pathogens and, in other work, Lactobacillus rhamnosus GG suppressed CCL20 expression from IECs exposed to flagellin or flagellated non-pathogenic Escherichia coli. 42 In addition to bacteria and bacterial components, CCL20 can be induced by IL1β, TNFα or IFNγ 38 which has been found in various epithelial cell lines, including our HCECs, responding to S. aureus. 16,17 CCL20 production was not induced in our studies by non-pathogenic L. lactis, supporting the notion that there are epithelial sensing mechanisms that are pathogen-specific.…”