NDLI: Shifting of immune responsiveness to house dust mite by influenza A infection: genomic insights.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	O'Byrne, Paul M. Kolbeck, Roland Husain, Mainul Jordana, Manel Stampfli, Martin R. Al-Garawi, Amal Humbles, Alison A. Ilieva, Dora Coyle, Anthony J.
Description	Country affiliation: Canada Author Affiliation: Al-Garawi A ( Division of Respiratory Diseases and Allergy, Center for Gene Therapeutics, McMaster University, Hamilton, Ontario L8S 4K1, Canada.)
Abstract	Respiratory viral infections have been associated with an increased incidence of allergic asthma. However, the mechanisms by which respiratory infections facilitate allergic airway disease are incompletely understood. We previously showed that exposure to a low dose of house dust mite (HDM) resulted in enhanced HDM-mediated allergic airway inflammation, and, importantly, marked airway hyperreactivity only when allergen exposure occurred during an acute influenza A infection. In this study, we evaluated the impact of concurrent influenza infection and allergen exposure at the genomic level, using whole-genome microarray. Our data showed that, in contrast to exposure to a low dose of HDM, influenza A infection led to a dramatic increase in gene expression, particularly of TLRs, C-type lectin receptors, several complement components, as well as FcÎµR1. Additionally, we observed increased expression of a number of genes encoding chemokines and cytokines associated with the recruitment of proinflammatory cells. Moreover, HDM exposure in the context of an influenza A infection resulted in the induction of unique genes, including calgranulin A (S100a8), an endogenous damage-associated molecular pattern and TLR4 agonist. In addition, we observed significantly increased expression of serum amyloid A (Saa3) and serine protease inhibitor 3n (Serpina3n). This study showed that influenza infection markedly increased the expression of multiple gene classes capable of sensing allergens and amplifying the ensuing immune-inflammatory response. We propose that influenza A infection primes the lung environment in such a way as to lower the threshold of allergen responsiveness, thus facilitating the emergence of a clinically significant allergic phenotype.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	2
Volume Number	188
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-01-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Genome, Viral Immunology Influenza A Virus, H1n1 Subtype Principal Component Analysis Pyroglyphidae Genetics Allergens Administration & Dosage Animals Gene Expression Regulation, Viral Mice Mice, Inbred Balb C Oligonucleotide Array Sequence Analysis Orthomyxoviridae Infections Pathology Virology Respiratory Hypersensitivity Signal Transduction Time Factors Research Support, Non-u.s. Gov't Validation Studies Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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