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Review
. 2016 Mar;137(3):659-65; quiz 666.
doi: 10.1016/j.jaci.2016.01.002.

The contributions of allergic sensitization and respiratory pathogens to asthma inception

Affiliations
Review

The contributions of allergic sensitization and respiratory pathogens to asthma inception

Daniel J Jackson et al. J Allergy Clin Immunol. 2016 Mar.

Abstract

Of the chronic diseases affecting grade-school children, asthma is the most common and accounts for the greatest number of school days missed. Moreover, it can influence family dynamics and function in other ways, and unfortunately, it can also be associated with mortality, particularly in the inner-city environments of the United States. Thus understanding factors that lead to its development in early life is essential in developing strategies aimed at primary prevention. Two risk factors that have been identified by a number of investigators include the development of allergic sensitization and wheezing respiratory tract illnesses caused by viruses and bacteria, either alone or in combination. Both of these factors appear to exert their influences within the first few years of life, such that asthma becomes established before the child enters grade school at age 5 to 6 years. Therefore, because both allergic sensitization and viral and bacterial illnesses can occur in children who do not have asthma, it is paramount to identify genetic and environmental factors that activate, interact with, and/or direct the immune system and components of the respiratory tract along pathways that allow asthma to become established and expressed clinically.

Keywords: Asthma; allergic sensitization; bacteria; childhood; inflammation; respiratory syncytial virus; rhinovirus; viruses.

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Figures

Fig 1
Fig 1
Interplay between FcεRI and antiviral responses. In normal airways plasmacytoid dendritic cells (pDCs) are major sources of type I and type III interferons in response to viral infections. These cells also have low-level expression of FcεRI. In the context of allergy, pDCs express greater FcεRI, which is inversely related to interferon responses. In addition, cross-linking of FcεRI further reduces interferon responses. Consequences of suppressed interferon responses to viral infection could include increased viral replication, more severe illnesses with wheezing, and exacerbation of pre-existing asthma.

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