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
Language
- eng
Conference Location
- Netherlands