Genetics and epidemiology: asthma and infection

Bartlett, Nathan W.; McLean, Gary R.; Chang, Yoon-Seok; Johnston, Sebastian L.

doi:10.1097/aci.0b013e32833066fa

Cited by 46 publications

(36 citation statements)

References 41 publications

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“…It should be noted, however, that the proportion of hospitalisations for asthma requiring admission to an intensive care unit remains constant relative to total admissions [22]. Other respiratory viruses responsible for exacerbations display different seasonal variation; respiratory syncytial virus (RSV) and influenza have been associated with increased asthma exacerbations during the winter months [23].…”

Section: Epidemiologymentioning

confidence: 99%

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Xepapadaki¹,

Papadopoulos²

2010

Eur Respir J

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Respiratory infections have been implicated in the origin and exacerbation of asthma in a variety of ways; however, systemisation of this knowledge in a way helpful for disease management remains suboptimal.Several conceptual issues need to be taken into account: the fact that the effects of an infection may vary according to genetic background, the current immune status of the host, and parallel environmental stimuli, in addition to the particular infectious agent itself. Moreover, childhood is a very special period because of the continuous processes taking place, such as neural, immune and respiratory maturation.Epidemiological studies have convincingly demonstrated that the majority of asthma exacerbations, in both adults and children, follow viral upper respiratory tract infections. Asthma exacerbations are still often unresponsive to current asthma treatment, and new therapeutic approaches are required.This review presents current knowledge on the associations between infection and exacerbation of established asthma with respect to definitions, epidemiology, mechanisms and treatment.

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Section: Epidemiologymentioning

confidence: 99%

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Xepapadaki¹,

Papadopoulos²

2010

Eur Respir J

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“…This suggests that the natural response to allergens is immunologic homeostasis and that additional factors contribute to triggering aberrant immune responses to these allergens (2). In addition to a genetic predisposition, environmental factors, such as respiratory viral infections, have been implicated with the clinical expression of allergic airway inflammation (3,4). In this regard, there is abundant evidence in humans of an association between viral infections and the expression of asthma (5,6).…”

mentioning

confidence: 99%

Shifting of Immune Responsiveness to House Dust Mite by Influenza A Infection: Genomic Insights

Al-Garawi

Husain

Ilieva

et al. 2012

The Journal of Immunology

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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 FcεR1. 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.

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“…It is not clear whether respiratory infection is a marker identifying infants with a predisposition to develop asthma, or whether infection is causally related to the inception of asthma [5,6]. Early life is a crucial period for lung development, and it has been argued that viral infection itself may actually increase the risk of asthma by influencing the development of immune response or by altering lung function [4,7,8].…”

mentioning

confidence: 99%

17q21 variants modify the association between early respiratory infections and asthma

Smit

Bouzigon

Pin³

et al. 2009

Eur Respir J

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Single nucleotide polymorphisms (SNPs) at chromosome 17q21 confer an increased risk of early-onset asthma. The objective was to study whether 17q21 SNPs modify associations between early respiratory infections and asthma.Association analysis was conducted in 499 children (268 with asthma, median age 11 yrs) from the Epidemiological Study on the Genetics and Environment of Asthma (EGEA). The 12-yr followup data were used to assess persistent or remittent asthma in young adulthood. Respiratory infection before 2 yrs of age was assessed retrospectively.For the 12 17q21 SNPs studied, the odds ratios (OR) for association between infection and early-onset asthma (age at onset f4 yrs) were higher in carriers of risk genotypes (OR 3.42-6.36) than in noncarriers (OR 1.84-2.44; p-value for interaction 0.02-0.04 for five SNPs). Risk genotypes also increased the association between infection and childhood asthma that remits in adulthood (OR 4.84-7.16 in carriers and 1.74-2.25 in noncarriers; p-value for interaction 0.008-0.05 for 10 SNPs). In children with 17q21 risk genotypes and early-life environmental tobacco smoke (ETS) exposure, associations between infection and asthma were further enhanced.17q21 genetic variants and early ETS exposure enhance the association between early respiratory infections and early-onset asthma and childhood asthma that remits in adulthood.

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Genetics and epidemiology: asthma and infection

Abstract: Early in life, such genetic factors contribute to the risk of severe lower respiratory tract viral infection as well as later development of wheezing illness and asthma. Respiratory viruses are also the most frequent cause of asthma exacerbations at all ages.

Cited by 46 publications

References 41 publications

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Childhood asthma and infection: virus-induced exacerbations as determinants and modifiers: Figure 1–

Shifting of Immune Responsiveness to House Dust Mite by Influenza A Infection: Genomic Insights

17q21 variants modify the association between early respiratory infections and asthma

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