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Role of CCR5 in the pathogenesis of IL-13-induced inflammation and remodeling

Bing Ma1, Wei Liu, Robert J Homer

  • 1Section of Pulmonary and Critical Care Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|April 6, 2006
PubMed

Insights

Interleukin-13 (IL-13) drives tissue damage by inducing the CCR5 receptor. Blocking CCR5 reduces IL-13-mediated inflammation, remodeling, and respiratory failure, highlighting CCR5

Area of Science:

  • Immunology and Inflammation Research
  • Respiratory Medicine
  • Molecular Biology

Background:

  • Interleukin-13 (IL-13) is a key cytokine in Th2-mediated inflammation and tissue remodeling.
  • The chemokine receptor CCR5 and its ligands are often present at sites of IL-13 activity.
  • The role of CCR5 in IL-13-induced pathogenesis remains to be fully elucidated.

Purpose of the Study:

  • To investigate the role of CCR5 in the development of IL-13-induced lung inflammation and tissue remodeling.
  • To determine if IL-13 influences CCR5 expression in the murine lung.
  • To assess the impact of CCR5 blockade or deficiency on IL-13-driven pathological outcomes.

Main Methods:

  • Evaluating CCR5 expression in response to IL-13 in murine lungs.
  • Comparing IL-13-induced responses in mice treated with anti-CCR5 antibodies versus controls.
  • Utilizing wild-type and CCR5-deficient mice to assess CCR5's role in IL-13 pathogenesis.
  • Analyzing the expression of chemokines, matrix metalloproteinases, cell death regulators, and caspases.

Main Results:

  • IL-13 significantly stimulates CCR5 expression in epithelial cells.
  • Neutralization or absence of CCR5 markedly reduces IL-13-induced inflammation, alveolar remodeling, apoptosis, and mortality.
  • CCR5 is essential for optimal IL-13-mediated induction of specific chemokines, MMP-9, and cell death pathways.
  • CCR5 is required for IL-13's effects on alpha1-antitrypsin inhibition and caspase activation.

Conclusions:

  • CCR5 plays a critical role in the pathogenesis of IL-13-induced lung inflammation and tissue remodeling.
  • Targeting CCR5 may offer a therapeutic strategy for IL-13-driven respiratory diseases.
  • IL-13 and CCR5 signaling pathways are intricately linked in the context of Th2 inflammation.

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