Strain-specific requirement for eosinophils in the recruitment of T cells to the lung during the development of allergic asthma

Elizabeth Rose Walsh, Nisebita Sahu, Jennifer Kearley, Ebony Benjamin, Hyon Kang Boo, Alison Humbles, Avery August

Research output: Contribution to journalArticle

112 Scopus citations

Abstract

Eosinophils have been implicated as playing a major role in allergic airway responses. However, the importance of these cells to the development of this disease has remained ambiguous despite many studies, partly because of lack of appropriate model systems. In this study, using transgenic murine models, we more clearly delineate a role for eosinophils in asthma. We report that, in contrast to results obtained on a BALB/c background, eosinophil-deficient C57BL/6 ΔdblGATA mice (eosinophil-null mice via the ΔDblGATA1 mutation) have reduced airway hyperresponsiveness, and cytokine production of interleukin (IL)-4, -5, and -13 in ovalbumin-induced allergic airway inflammation. This was caused by reduced T cell recruitment into the lung, as these mouse lungs had reduced expression of CCL7/MCP-3, CC11/eotaxin-1, and CCL24/eotaxin-2. Transferring eosinophils into these eosinophildeficient mice and, more importantly, delivery of CCL11/eotaxin-1 into the lung during the development of this disease rescued lung T cell infiltration and airway inflammation when delivered together with allergen. These studies indicate that on the C57BL/6 background, eosinophils are integral to the development of airway allergic responses by modulating chemokine and/or cytokine production in the lung, leading to T cell recruitment.

Original languageEnglish (US)
Pages (from-to)1285-1292
Number of pages8
JournalJournal of Experimental Medicine
Volume205
Issue number6
DOIs
StatePublished - Jun 9 2008

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Fingerprint Dive into the research topics of 'Strain-specific requirement for eosinophils in the recruitment of T cells to the lung during the development of allergic asthma'. Together they form a unique fingerprint.

  • Cite this