Chlamydia muridarum lung infection in infants alters hematopoietic cells to promote allergic airway disease in mice

Malcolm R Starkey, Richard Y Kim, Emma L Beckett, Heidi C Schilter, Doris SC Shim, Ama-Tawiah Essilfie, Duc H Nguyen, Kenneth W Beagley, Joerg Mattes, Charles R Mackay, Jay C Horvat, Philip M Hansbro

    Research output: Contribution to journalArticleResearchpeer-review

    22 Citations (Scopus)

    Abstract

    BACKGROUND: Viral and bacterial respiratory tract infections in early-life are linked to the development of allergic airway inflammation and asthma. However, the mechanisms involved are not well understood. We have previously shown that neonatal and infant, but not adult, chlamydial lung infections in mice permanently alter inflammatory phenotype and physiology to increase the severity of allergic airway disease by increasing lung interleukin (IL)-13 expression, mucus hyper-secretion and airway hyper-responsiveness. This occurred through different mechanisms with infection at different ages. Neonatal infection suppressed inflammatory responses but enhanced systemic dendritic cell:T-cell IL-13 release and induced permanent alterations in lung structure (i.e., increased the size of alveoli). Infant infection enhanced inflammatory responses but had no effect on lung structure. Here we investigated the role of hematopoietic cells in these processes using bone marrow chimera studies. METHODOLOGY/PRINCIPAL FINDINGS: Neonatal (
    Original languageEnglish
    Article numbere42588
    Number of pages7
    JournalPLoS ONE
    Volume7
    Issue number8
    DOIs
    Publication statusPublished - 2012

    Cite this