Local inflammation exacerbates the severity of Staphylococcus aureus skin infection

Christopher P Montgomery1, Melvin D Daniels, Fan Zhao

  • 1Department of Pediatrics, University of Chicago, Chicago, Illinois, USA. cmontgomery@bsd.uchicago.edu

Plos One
|July 18, 2013
PubMed

Insights

The severity of Staphylococcus aureus skin infections is driven by inflammation, not bacterial numbers. Athymic nude mice showed smaller lesions with less inflammation, independent of T cells.

Area of Science:

  • Immunology
  • Microbiology
  • Dermatology

Background:

  • Staphylococcus aureus is a primary cause of bacterial skin infections.
  • The relationship between bacterial burden and clinical severity in skin infections is not fully understood.

Purpose of the Study:

  • To investigate the role of the host inflammatory response in Staphylococcus aureus skin infection severity.
  • To determine if T cell deficiency influences lesion size and inflammatory markers.

Main Methods:

  • Comparison of lesion size and bacterial burden in athymic nude mice versus wild-type mice during S. aureus skin infection.
  • Measurement of myeloperoxidase, IL-17A, and CXCL1 levels in skin lesions.
  • Assessment of T cell deficiency impact using TCR βδ (-/-) mice and adoptive T cell transfer.

Main Results:

  • Lesion size did not correlate with bacterial burden in the mouse model.
  • Athymic nude mice exhibited smaller skin lesions with reduced myeloperoxidase, IL-17A, and CXCL1 levels compared to wild-type mice, despite similar bacterial loads.
  • T cell deficiency did not account for the observed differences in lesion size.

Conclusions:

  • The clinical severity of S. aureus skin infections is primarily dictated by the host's inflammatory response.
  • This inflammatory response appears to be T cell-independent in the context of skin infection severity.
  • Findings highlight the inflammatory component over bacterial load in driving S. aureus skin infection pathology.

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