Intrinsic AHR in IL-5 transgenic mice is dependent on C4+ cells and CD49d-mediated signaling

Michael T. Borchers, J. Crosby, P. Justice, S. Farmer, E. Hines, J. J. Lee, N. A. Lee

Research output: Contribution to journalArticle

17 Scopus citations

Abstract

Overexpression of interleukin (IL)-5 by the airway epithelium in mice using the rat CC10 promoter (NJ.1726 line) leads to several histopathologies characteristic of human asthma, including airway hyperreactivity (AHR). We investigated the contribution of B and T cells, as well as CD4 expression, to the development of AHR in IL-5 transgenic mice. NJ.1726 mice on a T cell or CD4 knockout background, but not on a B cell knockout background, lost intrinsic AHR. These effects occurred without decreases in IL-5 or eosinophils. We further investigated the contribution of α4-integrin signaling to the development of AHR in IL-5 transgenic mice through the administration of anti-CD49d (α4-integrin) antibody (PS/2). Administration of PS/2 resulted in immediate (16-h) inhibition of AHR. The inhibition of AHR was not associated with a decrease in airway eosinophils. These studies demonstrate that, despite the presence of increased levels of IL-5 and eosinophils in the lungs of NJ.1726 mice, CD4+ cells and α4-integrin signaling are necessary for the intrinsic AHR that develops in IL-5 transgenic mice.

Original languageEnglish (US)
Pages (from-to)L653-L659
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume281
Issue number3 25-3
DOIs
StatePublished - 2001

Keywords

  • Cytokines
  • Eosinophil
  • Inflammation
  • Interleukin-5
  • T cell

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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