Viral Infections, Cytokine Dysregulation and the Origins of Childhood Asthma and Allergic Diseases

Friedlander, Samuel L.; Jackson, Daniel J.; Gangnon, Ronald E.; Evans, Michael D.; Li, Zhanhai; Roberg, K.A.; Anderson, Elizabeth; Carlson-Dakes, K.; Adler, Kiva J.; Gilbertson‐White, Stephanie; Pappas, T.E.; DaSilva, D.F.; Tisler, C.J.; Pleiss, L.E.; Mikus, Lance D.; Rosenthal, Louis A.; Shult, Peter; Kirk, Carol J.; Reisdorf, Erik; Hoffjan, Sabine; Gern, James E.; Lemanske, Robert F.

doi:10.1097/01.inf.0000187273.47390.01

Cited by 45 publications

(39 citation statements)

References 69 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This would be consistent with the concept that early life exposures to pathogens that elicit Th1-biased immune responses protect offspring from development of allergic airway disease (21)(22)(23)(24)(25). To evaluate whether maternal transfer of Ag-independent factors contributed to the resistance of progeny of OVA-CFA mothers to OVA-induced allergic airway disease (see Fig.…”

Section: Th1-biased Immunity To Bsa Was Not Sufficient For Maternal Tmentioning

confidence: 66%

“…Although the concept as originally envisaged has been modified as the field evolved in the past 15 years, support remains for the idea that exposures to microbes could be important to direct maturation of the immune system in early life toward a healthy balance of Th1-and Th2-type immune responsiveness. Epidemiologic studies are supportive of this "hygiene hypothesis," whereby decreased exposure to other children, infectious diseases, or microbial products is associated with increased risk of allergic disease (22)(23)(24)(25). In addition, the ability of certain environmental conditions to increase or decrease asthma susceptibility, such as day care attendance or endotoxin exposure, can be transposed or eliminated based on parental history of atopy or asthma (26,27).…”

mentioning

confidence: 93%

See 1 more Smart Citation

Maternal Transmission of Resistance to Development of Allergic Airway Disease

Matson

Zhu

Lingenheld

et al. 2007

The Journal of Immunology

View full text Add to dashboard Cite

Parental phenotype is known to influence the inheritance of atopic diseases, such as allergic asthma, with a maternal history being a more significant risk factor for progeny than paternal history. We hypothesized that recall Th1- or Th2-type immune responses during pregnancy would result in transfer of maternal factors that would differentially impact development of immune responsiveness in offspring. Following weaning, susceptibility and severity of allergic airway disease (a murine model of human asthma) was evaluated in progeny, disease being elicited by immunization with OVA-Al(OH)3 and challenge with aerosolized OVA. We found that progeny of mothers with Th1-biased immunity to OVA subjected to recall aerosol challenge during pregnancy had reduced levels of Ag-specific IgE and airway eosinophilia compared with progeny of mothers with Th2-biased immunity to OVA or naive mothers. Interestingly, progeny of mothers with Th1-type immunity to a heterologous albumin, BSA, were not protected from developing OVA-induced allergic airway disease. These findings demonstrated that maternal transfer of protection from development of allergic airway disease to offspring in this model of maternal Th1-type immunity was Ag specific.

show abstract

Section: Th1-biased Immunity To Bsa Was Not Sufficient For Maternal Tmentioning

confidence: 66%

mentioning

confidence: 93%

Maternal Transmission of Resistance to Development of Allergic Airway Disease

Matson

Zhu

Lingenheld

et al. 2007

The Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…This controversy relates in part to small sample size, cross-sectional analysis, lack of precise case definition and incomplete microbial assessment in studies of this phenomenon. 110,111 Respiratory infections in early childhood are associated with early wheezing, 109 but it is unclear whether infection alone has a role in the development of persistent asthma.…”

Section: Antibiotics and Infectionsmentioning

confidence: 99%

“…Interactions of genes with environmental exposures (including allergens, air pollution, environmental tobacco smoke and diet) modulate the host response to infections. 108,109 It remains controversial whether the occurrence or timing of childhood infection is pathogenic or protective for the development and long-term outcome of asthma and allergy and of nonallergic wheeze phenotypes. This controversy relates in part to small sample size, cross-sectional analysis, lack of precise case definition and incomplete microbial assessment in studies of this phenomenon.…”

Section: Antibiotics and Infectionsmentioning

confidence: 99%

Asthma: epidemiology, etiology and risk factors

Subbarao¹,

Mandhane²,

Sears³

2009

Canadian Medical Association Journal

432

303

View full text Add to dashboard Cite

“…Several hypotheses have been advanced to explain the mechanisms that trigger asthma crises during respiratory infections (4)(5)(6)(7). Focused mainly on HRV-associated episodes, two nonexclusive theories attribute asthma attacks to direct viral injury and immune-mediated exacerbations (7)(8)(9)(10).…”

mentioning

confidence: 99%

A Mechanistic Role for Type III IFN-λ₁ in Asthma Exacerbations Mediated by Human Rhinoviruses

Miller

Hernandez

Wimmenauer

et al. 2012

Am J Respir Crit Care Med

View full text Add to dashboard Cite

Rationale: Human rhinoviruses (HRV) are the leading cause of upper respiratory infections and have been postulated to trigger asthma exacerbations. However, whether HRV are detected during crises because upper respiratory infections often accompany asthma attacks, or because they specifically elicit exacerbations, is unclear. Moreover, although several hypotheses have been advanced to explain virus-induced exacerbations, their mechanism remains unclear. Objectives: To determine the role of HRV in pediatric asthma exacerbations and the mechanisms mediating wheezing. Methods: We prospectively studied 409 children with asthma presenting with upper respiratory infection in the presence or absence of wheezing. Candidate viral and immune mediators of illness were compared among children with asthma with different degrees of severity of acute asthma. Measurements and Main Results: HRV infections specifically associated with asthma exacerbations, even after adjusting for relevant demographic and clinical variables defined a priori (odds ratio, 1.90; 95% confidence interval, 1.21-2.99; P ¼ 0.005). No difference in virus titers, HRV species, and inflammatory or allergic molecules was observed between wheezing and nonwheezing children infected with HRV. Type III IFN-l 1 levels were higher in wheezing children infected with HRV compared with nonwheezing (P , 0.001) and increased with worsening symptoms (P , 0.001). Moreover, after adjusting for IFN-l 1 , children with asthma infected with HRV were no longer more likely to wheeze than those who were HRV-negative (odds ratio, 1.18; 95% confidence interval, 0.57-2.46; P ¼ 0.66). Conclusions: Our findings suggest that HRV infections in children with asthma are specifically associated with acute wheezing, and that type III IFN-l 1 responses mediate exacerbations caused by HRV. Modulation of IFN-l 1 should be studied as a therapeutic target for exacerbations caused by HRV.Keywords: asthma; interferon-l; rhinovirus; children; asthma exacerbation Asthma exacerbations are the main cause of hospitalization in children, and occur in association with respiratory viral infections (1, 2). Human rhinoviruses (HRV) are frequently isolated in the upper airways of children during respiratory infections and during asthma attacks, and have been postulated to trigger these crises (3, 4). However, whether HRV are detected during asthma crises because they are the most frequent cause of upper respiratory infections (URI; which accompany asthma attacks), or because they can specifically elicit asthma exacerbations is unclear. To our knowledge, no pediatric study has compared the viral etiology of URI in patients with asthma with and without wheezing to investigate the specific association between HRV URI and asthma attacks.Several hypotheses have been advanced to explain the mechanisms that trigger asthma crises during respiratory infections (4-7). Focused mainly on HRV-associated episodes, two nonexclusive theories attribute asthma attacks to direct viral injury and immune-mediated exacerbations ...

show abstract

Viral Infections, Cytokine Dysregulation and the Origins of Childhood Asthma and Allergic Diseases

Abstract: Associations between clinical wheezing, viral identification, specific cytokine responses and genetic variation provide insight into the immunopathogenesis of childhood asthma and allergic diseases.

Cited by 45 publications

References 69 publications

Maternal Transmission of Resistance to Development of Allergic Airway Disease

Maternal Transmission of Resistance to Development of Allergic Airway Disease

Asthma: epidemiology, etiology and risk factors

A Mechanistic Role for Type III IFN-λ₁ in Asthma Exacerbations Mediated by Human Rhinoviruses

Contact Info

Product

Resources

About

Viral Infections, Cytokine Dysregulation and the Origins of Childhood Asthma and Allergic Diseases

Abstract: Associations between clinical wheezing, viral identification, specific cytokine responses and genetic variation provide insight into the immunopathogenesis of childhood asthma and allergic diseases.

Cited by 45 publications

References 69 publications

Maternal Transmission of Resistance to Development of Allergic Airway Disease

Maternal Transmission of Resistance to Development of Allergic Airway Disease

Asthma: epidemiology, etiology and risk factors

A Mechanistic Role for Type III IFN-λ1 in Asthma Exacerbations Mediated by Human Rhinoviruses

Contact Info

Product

Resources

About

A Mechanistic Role for Type III IFN-λ₁ in Asthma Exacerbations Mediated by Human Rhinoviruses