European Journal of Clinical Microbiology & Infectious Diseases

, Volume 29, Issue 6, pp 633–641

Eradication of the commensal intestinal microflora by oral antimicrobials interferes with the host response to lipopolysaccharide

Authors

  • T. Umenai
    • Department of Anesthesiology and Intensive Care, University HospitalKyoto Prefectural University of Medicine
  • H. Hirai
    • Department of Microbiology and ImmunologyKyoto Prefectural University of Medicine
    • Department of Anesthesiology and Intensive Care, University HospitalKyoto Prefectural University of Medicine
  • T. Nakaya
    • International Research Centre for Infectious Diseases, Research Institute for Microbial DiseasesOsaka University
  • T. Asahara
    • Yakult Central Institute for Microbiological Research
  • K. Nomoto
    • Yakult Central Institute for Microbiological Research
  • M. Kita
    • Department of Microbiology and ImmunologyKyoto Prefectural University of Medicine
  • Y. Tanaka
    • Department of Anesthesiology and Intensive Care, University HospitalKyoto Prefectural University of Medicine
  • J. Imanishi
    • Department of Microbiology and ImmunologyKyoto Prefectural University of Medicine
Article

DOI: 10.1007/s10096-010-0905-3

Cite this article as:
Umenai, T., Hirai, H., Shime, N. et al. Eur J Clin Microbiol Infect Dis (2010) 29: 633. doi:10.1007/s10096-010-0905-3

Abstract

The host components and commensal microorganisms of the intestinal microenvironment play roles in the development and maintenance of the host defence. Recent observations have suggested that toll-like receptors (TLRs) are involved in the recognition of innate immunity against intestinal microbes. However, little is known regarding the role of TLR in the maintenance of systemic host defence by intestinal microorganisms. We studied the expression and function of TLR4 and TLR2 on alveolar and peritoneal macrophages in mice after 3 weeks of oral administration of streptomycin and cefotaxime. After active treatment, the intestinal microorganisms were nearly completely eradicated, and the surface expression of TLR4 and TLR2 on the peritoneal macrophages was prominently downregulated. When the actively treated mice were challenged with lipopolysaccharide (LPS), a TLR4 ligand, the host response was markedly impaired. Our results suggest that the oral administration of antimicrobials downregulates the expression of surface TLR on the peritoneal macrophages and modulates the host immune responses against LPS by modifying the intestinal environment.

Copyright information

© Springer-Verlag 2010