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Review
. 2012 Aug;130(2):343-51.
doi: 10.1016/j.jaci.2012.05.056.

Response to infections in patients with asthma and atopic disease: an epiphenomenon or reflection of host susceptibility?

Affiliations
Review

Response to infections in patients with asthma and atopic disease: an epiphenomenon or reflection of host susceptibility?

Kristina M James et al. J Allergy Clin Immunol. 2012 Aug.

Abstract

Associations between respiratory tract infections and asthma inception and exacerbations are well established. Infant respiratory syncytial virus and rhinovirus infections are known to be associated with an increased risk of asthma development, and among children with prevalent asthma, 85% of asthma exacerbations are associated with viral infections. However, the exact nature of this relationship remains unclear. Is the increase in severity of infections an epiphenomenon, meaning respiratory tract infections just appear to be more severe in patients with underlying respiratory disease, or instead a reflection of altered host susceptibility among persons with asthma and atopic disease? The main focus of this review is to summarize the available levels of evidence supporting or refuting the notion that patients with asthma or atopic disease have an altered susceptibility to selected pathogens, as well as discussing the biological mechanism or mechanisms that might explain such associations. Finally, we will outline areas in need of further research because understanding the relationships between infections and asthma has important implications for asthma prevention and treatment, including potential new pathways that might target the host immune response to select pathogens.

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Figures

Fig 1
Fig 1
Levels of clinical evidence to support an increased risk and host susceptibility to infections in the asthmatic and atopic host. LRTI, Lower respiratory tract infections; RV, rhinovirus; URI, upper respiratory tract infection.
Fig 2
Fig 2
Biological mechanisms that explain an altered immune response to viral and bacterial infections in the asthmatic and atopic host.

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