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Macrophages from patients with atopic dermatitis show a reduced CXCL10 expression in response to staphylococcal

S Kasraie1, M Niebuhr, V Kopfnagel

  • 1Division of Immunodermatology and Allergy Research, Department of Dermatology and Allergy, Hannover Medical School, Carl-Neuburg-Strasse 1, Hannover,Germany. kasraie.sadaf@mh-hannover.de

Allergy
|September 13, 2011
PubMed
Abstract

Insights

Staphylococcal alpha-toxin induces CXCL10 in macrophages, promoting Th1 polarization. Macrophages from atopic dermatitis (AD) patients showed varied CXCL10 responses compared to psoriasis patients and controls.

Area of Science:

  • Immunology
  • Dermatology
  • Microbiology

Background:

  • Atopic dermatitis (AD) and psoriasis patients often harbor Staphylococcus aureus (S. aureus).
  • S. aureus alpha-toxin is linked to AD severity.
  • Distinct chemokine profiles (CCL, CXCL) are observed in AD and psoriasis.

Purpose of the Study:

  • Investigate sublytic alpha-toxin effects on human macrophages in AD and psoriasis.
  • Analyze the impact of alpha-toxin on chemokine production and immune cell recruitment.

Main Methods:

  • Quantified IFN-γ-induced protein of 10-kDa (IP-10)/CXCL10 and macrophage-derived chemokine (MDC)/CCL22 via qRT-PCR and ELISA.
  • Assessed cell surface markers and chemotaxis using flow cytometry and Boyden chamber assays.

Main Results:

  • Alpha-toxin significantly induced CXCL10 (mRNA and protein) and upregulated MHC class II in macrophages.
  • Alpha-toxin-stimulated macrophages promoted CD4+ lymphocyte migration via CXCL10/CXCR3.
  • Macrophages from AD patients produced less CXCL10 in response to alpha-toxin compared to psoriasis patients and controls.
  • CCL22 production showed minimal variation across groups.

Conclusions:

  • Staphylococcal alpha-toxin drives Th1 polarization through CXCL10 induction in macrophages.
  • Differential CXCL10 responses to alpha-toxin in AD and psoriasis macrophages may influence skin leukocyte recruitment.

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