Pseudomonas aeruginosa-dependent upregulation of TLR2 influences host responses to a secondary Staphylococcus aureus infection

Pathog Dis. 2013 Nov;69(2):149-56. doi: 10.1111/2049-632X.12074. Epub 2013 Sep 2.

Abstract

The clinical impact of polymicrobial infections has received increasing attention from the medical community. However, the potential effects of Pseudomonas aeruginosa infection on the development of host responses against Gram-positive bacteria, such as Staphylococcus aureus, are unknown. Here, P. aeruginosa infection was found to induce the expression of Toll-like receptor 2 (TLR2), which plays a dominant role in sensing pathogen-associated molecular patterns (PAMPs) expressed by Gram-positive bacteria. P. aeruginosa-dependent upregulation of TLR2 was not mediated by flagellin, or by the type III (T3SS) or type VI (T6SS) secretion systems, but was upregulated by lipopolysaccharide (LPS). Upregulation of TLR2 influenced the magnitude of proinflammatory responses to the secondary S. aureus infection, but there was no clear effect on phagocytosis of S. aureus by macrophages. Taken together, the results of this study demonstrate that P. aeruginosa infection results in the upregulation of TLR2 expression, subsequently enhancing innate immune responses against a secondary S. aureus infection.

Keywords: Pseudomonas aeruginosa; Staphylococcus aureus; TLR2; secondary infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Host-Pathogen Interactions*
  • Lipopolysaccharides / immunology
  • Macrophages / immunology*
  • Macrophages / microbiology*
  • Mice
  • Phagocytosis
  • Pseudomonas aeruginosa / immunology*
  • Staphylococcal Infections / immunology*
  • Toll-Like Receptor 2 / biosynthesis
  • Toll-Like Receptor 2 / immunology*
  • Up-Regulation

Substances

  • Lipopolysaccharides
  • TLR2 protein, human
  • Toll-Like Receptor 2