Family history of atopy and clinical course of RSV infection in ambulatory and hospitalized infants

Trefny, Ph.; Stricker, Tamar; Baerlocher, C; Sennhauser, FH

doi:10.1002/1099-0496(200010)30:4<302::aid-ppul5>3.0.co;2-r

Cited by 52 publications

(41 citation statements)

References 24 publications

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“…Complementary to this, we found the risk of RSV hospitalization was increased 3-fold to 4-fold in twins with asthma, independent of the time since the debut of asthma. This is in accordance with recent studies showing that asthmatic disposition and early wheezing increased the risk of severe lower respiratory tract infections and RSV hospitalization, [14][15][16][17] probably because of airway hyperresponsiveness.…”

Section: Discussionmentioning

confidence: 99%

“…[9][10][11] One particular cohort reported an asthma rate by age 13 years of 43% versus 8% and sensitization to common allergens in 45% versus 26% in children with infant hospitalization for RSV bronchiolitis compared with a matched control group. 12,13 On the other hand, predisposition to asthma and atopy was associated with an increased risk of lower respiratory tract infection and RSV hospitalization, [14][15][16] and early wheezy symptoms were found to be a strong risk factor for subsequent RSV hospitalization. 17 Impaired pulmonary function at 1 month of age increased the risk of wheezing episodes and asthma [18][19][20] and has been suspected to increase the risk of severe reaction to viral infection.…”

mentioning

confidence: 99%

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The causal direction in the association between respiratory syncytial virus hospitalization and asthma

Stensballe

Simonsen

Thomsen

et al. 2009

Journal of Allergy and Clinical Immunology

109

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

The causal direction in the association between respiratory syncytial virus hospitalization and asthma

Stensballe

Simonsen

Thomsen

et al. 2009

Journal of Allergy and Clinical Immunology

109

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“…Long-term follow-up studies have shown that wheezy episodes associated with rhinovirus infection are a strong predictor of asthma by the age of 6 years [22,23]. However, studies have also reported that children with early wheezy symptoms and a predisposition to asthma and atopy are at increased risk of lower respiratory infection [24][25][26]. Therefore, the direction of causality of viral infection and the development of asthma is still unclear.…”

Section: Childhood-onset Asthmamentioning

confidence: 95%

Adult-onset asthma: is it really different?

Nijs¹,

Venekamp²,

Bel³

2013

European Respiratory Review

246

205

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Asthma that starts in adulthood differs from childhood-onset asthma in that it is often non-atopic, more severe and associated with a faster decline in lung function.Understanding of the underlying mechanism of adult-onset asthma and identification of specific phenotypes may further our understanding of pathophysiology and treatment response, leading to better targeting of both existing and new approaches for personalised management. Pivotal studies in past years have led to sustained progress in many areas, ranging from risk factors for development, identification of different phenotypes, and introduction of new therapies.This review highlights and discusses literature on adult-onset asthma, with special focus on the differences from childhood-onset asthma, risk factors for development, phenotypes of adultonset asthma and new approaches for personalised management.

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“…With respect to the infection component in the scheme, the relevant recent observations are as follows: 1) genetic risk for atopy has been reported to be associated with increased susceptibility to severe RSV infection and bronchiolitis [61]; atopy in children has also been linked to increased susceptibility to measles-mumps-rubella [62] as well as to frequent upper respiratory tract infections [63]; 2) IFN-c responses in peripheral blood mononuclear cells are attenuated during acute RSV infection in children who develop bronchiolitis [59][60][61][62][63][64][65][66][67][68][69], suggesting that downregulated Th1 function may be associated with pathogenesis; 3) susceptibility to development of acute RSV bronchiolitis during infancy is associated with decreased levels of IL-12 in cord blood relative to subjects who do not develop bronchiolitis [70], suggesting a pre-existing deficiency in Th1 function in this group; 4) nonatopic wheezing children, in whom the principal stimulus for wheeze is viral infection per se, also have manifest reduced IFN-c responses [71]; and 5) a recent study by the authors9 group on a prospective cohort of infants followed to 18 months indicated that the development of T-cell memory to RSV (as a surrogate marker for RSV infection) during the observation period was inversely related to kinetics of postnatal maturation of IFN-c responses [72].…”

Section: The Apparent Dualistic Effects Of Respiratory Tract Infectiomentioning

confidence: 99%

Interactions between respiratory tract infections and atopy in the aetiology of asthma

Holt

Sly²

2002

European Respiratory Journal

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The prevalence of asthma, in particular atopic asthma, has markedly increased in recent years. Accumulating evidence suggests that environmental factors associated with allergic sensitization and exposure to microbial stimuli during infancy and early childhood, are associated with these changes in prevalence. However, considerable controversy surrounds the role of microbial agents, as evidence has been presented for both positive and negative effects in this context.The review below focuses upon interactions between immune competence during infancy, the development of T-helper (Th)1-polarized versus Th2-polarized memory against inhalant allergens, and susceptibility to virus infection. In particular, recent finding are highlighted which suggest that delayed postnatal maturation of Th1 function is associated with increased risk for early postnatal sensitization to inhalant allergens, and also with risk for viral bronchiolitis during infancy.Variations in the kinetics of postnatal maturation of T-helper 1 function may in part be attributable to polymorphisms in the CD14 gene, which influence host responsiveness both to bacterial as well as viral stimuli. It is evident from a wide range of studies carried out in different geographical areas, that the prevalence of allergic diseases, and in particular atopic asthma, has increased markedly over the last 2-3 decades. Moreover, the increases become evident in successive birth cohorts during early childhood. It is also generally accepted that "diagnostic shift" is not a significant factor in these changes. Accordingly, given the timeframe over which the changes have occurred, the responsible factor(s) must be environmental, presumably interacting with one or more susceptibility genes.The search for the relevant genetic and environmental factors continues, and a variety of potential candidates have been identified. Prominent amongst these are factors related to respiratory infections, particularly those occurring in childhood. Paradoxically, these infections have been invoked both as potential protective factors in relation to asthma/ allergy development, and as triggers of asthma exacerbations in atopic asthmatics. The mechanisms by which these effects may be mediated are incompletely understood; however, recent findings suggest some intriguing new possibilities, which are discussed in this review. T-cell immunity to inhalant allergens: the basis of variations in responder phenotype within the adult populationThe epithelial surface of the upper and lower respiratory tract are continuously exposed to an array of pathogenic and nonpathogenic airborne antigens, and the induction and local expression of local T-cell immunity must accordingly be tightly controlled, in order to avoid the pathological consequences of chronic T-cell-driven inflammation. While it is highly plausible that resistance to airborne pathogens is a direct function of the speed of mobilization and the intensity of expression of local innate and adaptive immune mechanisms in the lung, the conve...

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Family history of atopy and clinical course of RSV infection in ambulatory and hospitalized infants

Cited by 52 publications

References 24 publications

The causal direction in the association between respiratory syncytial virus hospitalization and asthma

The causal direction in the association between respiratory syncytial virus hospitalization and asthma

Adult-onset asthma: is it really different?

Interactions between respiratory tract infections and atopy in the aetiology of asthma

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