NDLI: Chlamydial respiratory infection during allergen sensitization drives neutrophilic allergic airways disease.

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Chlamydial respiratory infection during allergen sensitization drives neutrophilic allergic airways disease.

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Chlamydial respiratory infection during allergen sensitization drives neutrophilic allergic airways disease.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Preston, Julie A. Hansbro, Philip M. Kim, Richard Y. Beagley, Kenneth W. Horvat, Jay C. Gibson, Peter G. Foster, Paul S. Starkey, Malcolm R.
Description	Country affiliation: Australia Author Affiliation: Horvat JC ( Centre for Asthma and Respiratory Disease and Hunter Medical Research Institute, The University of Newcastle, Newcastle, New South Wales, Australia.)
Abstract	Neutrophilic asthma is a prevalent, yet recently described phenotype of asthma. It is characterized by neutrophilic rather than eosinophilic airway inflammation and airways hyperresponsiveness (AHR) and may have an infectious origin. Chlamydial respiratory infections are associated with asthma, but how these Th1-inducing bacteria influence Th2-mediated asthma remains unknown. The effects of chlamydial infection on the development of asthma were investigated using a BALB/c mouse model of OVA-induced allergic airways disease (AAD). The effects of current and resolved Chlamydia muridarum infection during OVA sensitization on AAD were assessed and compared with uninfected and nonsensitized controls. Current, but not resolved, infection attenuated hallmark features of AAD: pulmonary eosinophil influx, T cell production of IL-5, mucus-secreting cell hyperplasia, and AHR. Current infection also induced robust OVA-driven neutrophilic inflammation and IFN-gamma release from T cells. The phenotype of suppressed but persistent Th2 responses in association with enhanced neutrophilia is reminiscent of neutrophilic asthma. This phenotype was also characterized by increased pulmonary IL-12 and IL-17 expression and activation of APCs, as well as by reduced thymus- and activation-regulated chemokine. Inhibition of pulmonary neutrophil influx during infection blocked OVA-induced neutrophilic inflammation and T cell IFN-gamma production and reversed the suppressive effects on mucus-secreting cell hyperplasia and AHR during AAD. These changes correlated with decreased IL-12 and IL-17 expression, increased thymus- and activation-regulated chemokine and altered APC activation. Blocking IFN-gamma and IL-17 during OVA challenge had no effect. Thus, active chlamydial respiratory infection during sensitization enhances subsequent neutrophilic inflammation and Th1/Th17 responses during allergen exposure and may have a role in the pathogenesis of neutrophilic asthma.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	8
Volume Number	184
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2010-04-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Allergens Administration & Dosage Immunology Asthma Pathology Chlamydia Infections Chlamydia Muridarum Neutrophil Infiltration Respiratory Hypersensitivity Animals Microbiology Disease Models, Animal Immunophenotyping Inflammation Mice Mice, Inbred Balb C Neutrophils Ovalbumin Th1 Cells Th2 Cells Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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