title: Lactobacillus rhamnosus GG and Lactobacillus casei suppress Escherichia coli-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.
authors: Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan.
authors: Shinji
authors: S
authors: Toki
authors: Shinji
authors: S
authors: Kagaya
authors: Miwa
authors: M
authors: Shinohara
authors: Hiroshi
authors: H
authors: Wakiguchi
authors: Takashi
authors: T
authors: Matsumoto
authors: Yoshihisa
authors: Y
authors: Takahata
authors: Fumiki
authors: F
authors: Morimatsu
authors: Hirohisa
authors: H
authors: Saito
authors: Kenji
authors: K
authors: Matsumoto
mesh_terms: D002087:Butyrates / Q000494:pharmacology; D018938:Caco-2 Cells; D018925:Chemokines / Q000096:biosynthesis* / Q000235:genetics / Q000276:immunology; D004847:Epithelial Cells / Q000276:immunology / Q000382:microbiology; D004926:Escherichia coli / Q000276:immunology*; D006360:Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D007413:Intestinal Mucosa / Q000276:immunology* / Q000382:microbiology; D007780:Lacticaseibacillus casei / Q000502:physiology*; D052201:Lacticaseibacillus rhamnosus / Q000502:physiology*; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000276:immunology* / Q000378:metabolism
chemical_list: D002087:Butyrates; D018925:Chemokines; D006360:Heat-Shock Proteins; D051193:Toll-Like Receptors