Baseline airway hyperreactivity in A/J mice is not mediated by cells of the adaptive immune system

Husein Hadeiba, David B. Corry, Richard M. Locksley

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

Abstract

Human asthma is characterized by increased airway hyperreactivity to a variety of bronchoconstricting agents. Aberrant type 2 immune responses in the lung have been associated with airway hyperreactivity in both human asthma and in murine models of allergic airways disease. Despite their intrinsically elevated basal airway reactivity to smooth muscle constricting agents, A/J mice demonstrated no inherent inflammatory cell infiltration nor elevation of type 2 cytokines in the lung. Crossed bone marrow reconstitution experiments between A/J and MHC congenic B10.A mice revealed enhanced airway reactivity only in A/J recipients, irrespective of whether they had been reconstituted with A/J or B10.A hemopoietic cells. Further, A/J-derived bone marrow cells did not affect the reactivity of B10.A recipients. Although mice on RAG-deficient and IL-4-deficient backgrounds demonstrate substantial abrogation of allergen-induced airway hyperreactivity, these gene deletions had no impact on the elevated baseline reactivity when backcrossed onto A/J mice. Thus, in these mice, basal airway hyperreactivity is maintained independently of type 2 immunity induced by allergens.

Original languageEnglish (US)
Pages (from-to)4933-4940
Number of pages8
JournalJournal of Immunology
Volume164
Issue number9
DOIs
StatePublished - May 1 2000

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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