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

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 perm...

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Published in:PloS one 2012-08, Vol.7 (8), p.e42588-e42588
Main Authors: Starkey, Malcolm R, Kim, Richard Y, Beckett, Emma L, Schilter, Heidi C, Shim, Doris, Essilfie, Ama-Tawiah, Nguyen, Duc H, Beagley, Kenneth W, Mattes, Joerg, Mackay, Charles R, Horvat, Jay C, Hansbro, Philip M
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Language:English
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Summary: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. Neonatal (
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0042588