Toll-like receptor 2-dependent and -independent activation of macrophages by group B streptococci.

Journal Article (Journal Article)

Group B streptococcus (GBS), a capsulated gram-positive bacterium, is a major cause of newborn infections. Although the innate immune receptor Toll-like receptor (TLR) 2 has been shown to primarily recognize gram-positive bacterial products, the production of TNF by macrophages treated with heat-killed GBS (HK-GBS) does not depend on TLR2. In this report, we have characterized HK-GBS-induced activation of macrophages derived from wildtype and TLR2-deficient mice. Microarray analysis demonstrated that HK-GBS activation of macrophages induces both TLR2-independent and -dependent signals. While the expression of a major fraction of genes in macrophages induced by HK-GBS does not depend on TLR2, induction of several important molecules involved in host innate immunity such as IL-6, IL-1beta, and lipocalin 2 is severely impaired in the absence of TLR2 signaling. Furthermore, we show that HK-GBS utilizes centrifugation sensitive components to induce rapid activation of TLR2(-/-) macrophages and that HK-GBS-induced activation of macrophages is not mediated through its genomic DNA. Together, our results demonstrate that HK-GBS induces TLR2-dependent antimicrobial gene activation and provide further understanding of the molecular basis of host innate response to GBS infection.

Full Text

Duke Authors

Cited Authors

  • Draper, DW; Bethea, HN; He, Y-W

Published Date

  • February 15, 2006

Published In

Volume / Issue

  • 102 / 2

Start / End Page

  • 202 - 214

PubMed ID

  • 16242782

International Standard Serial Number (ISSN)

  • 0165-2478

Digital Object Identifier (DOI)

  • 10.1016/j.imlet.2005.09.005


  • eng

Conference Location

  • Netherlands