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Scavenger receptor A is expressed by macrophages in response to Porphyromonas gingivalis, and participates in

M T Baer1, N Huang, F C Gibson

  • 1Section of Infectious Diseases, Department of Medicine, Boston University School of Medicine, Boston, MA, USA.

Oral Microbiology and Immunology
|October 17, 2009
PubMed
Abstract

Insights

The scavenger receptor A (SR-A) is expressed by macrophages in response to Porphyromonas gingivalis. SR-A plays a role in macrophage production of tumor necrosis factor-alpha (TNF-alpha) during infection.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Porphyromonas gingivalis is a key bacterium in aggressive periodontal disease.
  • Pattern recognition receptors (PRRs) mediate host responses to P. gingivalis.
  • The role of scavenger receptor A (SR-A) in this response was investigated.

Purpose of the Study:

  • To investigate the expression and function of scavenger receptor A (SR-A) in macrophages during Porphyromonas gingivalis infection.
  • To determine SR-A's role in the production of inflammatory mediators like TNF-alpha.

Main Methods:

  • Quantitative reverse transcription PCR (qRT-PCR) to measure msr1 gene expression.
  • Flow cytometry to assess surface expression of SR-A protein.
  • Macrophage cultures using live, heat-killed, or mutant P. gingivalis, and purified capsular polysaccharide.
  • Experiments with SR-A knockout (SR-A(-/-)) macrophages and wild-type macrophages.

Main Results:

  • P. gingivalis infection increased msr1 gene and SR-A protein expression in macrophages.
  • SR-A expression was induced by heat-killed bacteria and capsular polysaccharide, not requiring live organisms.
  • Low-density lipoprotein (LDL) did not affect SR-A expression in response to P. gingivalis.
  • SR-A knockout macrophages produced significantly more TNF-alpha than wild-type macrophages when cultured with P. gingivalis.

Conclusions:

  • Scavenger receptor A (SR-A) is expressed by macrophages upon encountering P. gingivalis.
  • SR-A influences macrophage TNF-alpha production in response to P. gingivalis.

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