Evidence of infectious asthma phenotype: Chlamydia-induced allergy and pathogen-specific IgE in a neonatal mouse model.

Asthma is a chronic respiratory disease whose etiology is poorly understood. Recent studies suggest that early-life respiratory infections with atypical bacteria may play an important role in the induction or exacerbation of chronic respiratory disease. The current study utilized a neonatal mouse ov...

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Autores principales:	Katir K Patel, Wilmore C Webley
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/ef149e9b873e479b968a15ea8b5eb367
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spelling	oai:doaj.org-article:ef149e9b873e479b968a15ea8b5eb3672021-11-18T08:40:53ZEvidence of infectious asthma phenotype: Chlamydia-induced allergy and pathogen-specific IgE in a neonatal mouse model.1932-620310.1371/journal.pone.0083453https://doaj.org/article/ef149e9b873e479b968a15ea8b5eb3672013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24376704/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Asthma is a chronic respiratory disease whose etiology is poorly understood. Recent studies suggest that early-life respiratory infections with atypical bacteria may play an important role in the induction or exacerbation of chronic respiratory disease. The current study utilized a neonatal mouse ovalbumin (OVA) sensitization model of asthma to determine the course of early-life respiratory tract infection by Chlamydia. Neonatal (day 1) and adult (6 wks) BALB/c mice were infected intranasally with Chlamydia (MoPn) and 7 weeks later were sensitized and challenged with ovalbumin. Allergic airway disease was characterized by examination of serum and bronchoalveolar lavage fluid (BAL) cellularity, cytokine production and antibody response. The presence of Chlamydia was determined by PCR and culture. Ova-specific IgE was quantified by ELISA and Chlamydia-specific IgE was determined via Western blot analysis. Chlamydial infection in neonatal mice induced increased production of Th2 cytokines (IL-4, 5, 10, and 13) in both BAL and serum, while infected adult mice produced increased Th1 cytokines (IL-2, IFN-γ). The BAL from infected neonates contained significantly elevated levels of eosinophils compared to infected adult mice. Although adult mice cleared the infection ∼30 days post infection (pi), neonates were still infected 66 days after initial infection. Chlamydia-specific IgE was detected in both the BAL and serum of neonatal mice beginning 28 days post infection, however, infected adult mice did not produce Chlamydia-specific IgE antibodies over the course of the study. When allergic airway was induced using Ova, infected neonatal mice increased their production of IL-4, IL-5 and IL-13 by >2 fold compared to uninfected controls and infected adult groups. Our findings demonstrate that early-life Chlamydia infection induces a Th2-dominant cytokine response in the airways of neonatal mice, leading to chronic infection. More significantly, early life respiratory colonization with Chlamydia elicits pathogen-specific IgE production, which further supports an infectious asthma phenotype.Katir K PatelWilmore C WebleyPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 12, p e83453 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Katir K Patel Wilmore C Webley Evidence of infectious asthma phenotype: Chlamydia-induced allergy and pathogen-specific IgE in a neonatal mouse model.
description	Asthma is a chronic respiratory disease whose etiology is poorly understood. Recent studies suggest that early-life respiratory infections with atypical bacteria may play an important role in the induction or exacerbation of chronic respiratory disease. The current study utilized a neonatal mouse ovalbumin (OVA) sensitization model of asthma to determine the course of early-life respiratory tract infection by Chlamydia. Neonatal (day 1) and adult (6 wks) BALB/c mice were infected intranasally with Chlamydia (MoPn) and 7 weeks later were sensitized and challenged with ovalbumin. Allergic airway disease was characterized by examination of serum and bronchoalveolar lavage fluid (BAL) cellularity, cytokine production and antibody response. The presence of Chlamydia was determined by PCR and culture. Ova-specific IgE was quantified by ELISA and Chlamydia-specific IgE was determined via Western blot analysis. Chlamydial infection in neonatal mice induced increased production of Th2 cytokines (IL-4, 5, 10, and 13) in both BAL and serum, while infected adult mice produced increased Th1 cytokines (IL-2, IFN-γ). The BAL from infected neonates contained significantly elevated levels of eosinophils compared to infected adult mice. Although adult mice cleared the infection ∼30 days post infection (pi), neonates were still infected 66 days after initial infection. Chlamydia-specific IgE was detected in both the BAL and serum of neonatal mice beginning 28 days post infection, however, infected adult mice did not produce Chlamydia-specific IgE antibodies over the course of the study. When allergic airway was induced using Ova, infected neonatal mice increased their production of IL-4, IL-5 and IL-13 by >2 fold compared to uninfected controls and infected adult groups. Our findings demonstrate that early-life Chlamydia infection induces a Th2-dominant cytokine response in the airways of neonatal mice, leading to chronic infection. More significantly, early life respiratory colonization with Chlamydia elicits pathogen-specific IgE production, which further supports an infectious asthma phenotype.
format	article
author	Katir K Patel Wilmore C Webley
author_facet	Katir K Patel Wilmore C Webley
author_sort	Katir K Patel
title	Evidence of infectious asthma phenotype: Chlamydia-induced allergy and pathogen-specific IgE in a neonatal mouse model.
title_short	Evidence of infectious asthma phenotype: Chlamydia-induced allergy and pathogen-specific IgE in a neonatal mouse model.
title_full	Evidence of infectious asthma phenotype: Chlamydia-induced allergy and pathogen-specific IgE in a neonatal mouse model.
title_fullStr	Evidence of infectious asthma phenotype: Chlamydia-induced allergy and pathogen-specific IgE in a neonatal mouse model.
title_full_unstemmed	Evidence of infectious asthma phenotype: Chlamydia-induced allergy and pathogen-specific IgE in a neonatal mouse model.
title_sort	evidence of infectious asthma phenotype: chlamydia-induced allergy and pathogen-specific ige in a neonatal mouse model.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/ef149e9b873e479b968a15ea8b5eb367
work_keys_str_mv	AT katirkpatel evidenceofinfectiousasthmaphenotypechlamydiainducedallergyandpathogenspecificigeinaneonatalmousemodel AT wilmorecwebley evidenceofinfectiousasthmaphenotypechlamydiainducedallergyandpathogenspecificigeinaneonatalmousemodel
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Evidence of infectious asthma phenotype: Chlamydia-induced allergy and pathogen-specific IgE in a neonatal mouse model.

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