Recognition of Staphylococcus aureus-derived peptidoglycan (PGN) but not intact bacteria is mediated by CD14 in microglia

Nilufer Esen, Tammy L Kielian

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Recognition of Staphylococcus aureus and its cell-wall component peptidoglycan (PGN) by microglia is mediated, in part, by Toll-like receptor 2 (TLR2). However, the pattern recognition receptor (PRR) CD14 can also bind PGN and enhance TLR2-mediated signaling in macrophages, suggesting a similar phenomenon might occur in microglia. To assess the functional significance of CD14 on microglial activation, we evaluated the responses of primary microglia isolated from CD14 knockout (KO) and wild type (WT) mice. PGN-dependent microglial activation was partially CD14-dependent as demonstrated by the attenuated expression of TNF-α, macrophage inflammatory protein-2 (MIP-2/CXCL2), and the soluble PRR pentraxin-3 in CD14 KO microglia compared to WT cells. In contrast, microglial responses to intact S. aureus occurred primarily via a CD14-independent manner. Collectively, these findings reveal the complex nature of gram-positive bacterial recognition by microglia, which occurs, in part, via CD14.

Original languageEnglish (US)
Pages (from-to)93-104
Number of pages12
JournalJournal of Neuroimmunology
Volume170
Issue number1-2
DOIs
StatePublished - Dec 30 2005

Fingerprint

Peptidoglycan
Microglia
Staphylococcus aureus
Bacteria
Pattern Recognition Receptors
Toll-Like Receptor 2
Chemokine CXCL2
Cellular Structures
Knockout Mice
Cell Wall
Macrophages

Keywords

  • CD14
  • Central nervous system
  • Lipopolysaccharide
  • Microglia
  • Pentraxin-3
  • Peptidoglycan
  • S. aureus

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology

Cite this

Recognition of Staphylococcus aureus-derived peptidoglycan (PGN) but not intact bacteria is mediated by CD14 in microglia. / Esen, Nilufer; Kielian, Tammy L.

In: Journal of Neuroimmunology, Vol. 170, No. 1-2, 30.12.2005, p. 93-104.

Research output: Contribution to journalArticle

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