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

doi:10.1371/journal.pone.0042588

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

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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 language	English
Article number	e42588
Number of pages	7
Journal	PLoS ONE
Volume	7
Issue number	8
DOIs	https://doi.org/10.1371/journal.pone.0042588
Publication status	Published - 2012

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Starkey, M. R., Kim, R. Y., Beckett, E. L., Schilter, H. C., Shim, D. SC., Essilfie, A.-T., Nguyen, D. H., Beagley, K. W., Mattes, J., Mackay, C. R., Horvat, J. C., & Hansbro, P. M. (2012). Chlamydia muridarum lung infection in infants alters hematopoietic cells to promote allergic airway disease in mice. PLoS ONE, 7(8), Article e42588. https://doi.org/10.1371/journal.pone.0042588

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title = "Chlamydia muridarum lung infection in infants alters hematopoietic cells to promote allergic airway disease in mice",

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 (",

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AU - Starkey, Malcolm R

AU - Kim, Richard Y

AU - Beckett, Emma L

AU - Schilter, Heidi C

AU - Shim, Doris SC

AU - Essilfie, Ama-Tawiah

AU - Nguyen, Duc H

AU - Beagley, Kenneth W

AU - Mattes, Joerg

AU - Mackay, Charles R

AU - Horvat, Jay C

AU - Hansbro, Philip M

PY - 2012

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N2 - 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 (

AB - 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 (

UR - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3411632/pdf/pone.0042588.pdf

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DO - 10.1371/journal.pone.0042588

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

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