Patterns of allergic respiratory disease in children with a past history of bronchiolitis

Zweiman, Burton; Schoenwetter, William F.; Pappano, Joseph E.; Tempest, Bruce; Hildreth, Eugene A.

doi:10.1016/0091-6749(71)90029-7

Cited by 48 publications

(14 citation statements)

References 13 publications

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“…From clinical studies (9,10,33), respiratory viral infection has been suggested to contribute to the development of asthma. Previous studies (28,32) demonstrated that infection with influenza A virus enhances airway sensitization with antigen in mice.…”

Section: Discussionmentioning

confidence: 99%

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Immune Response Induced by Airway Sensitization after Influenza A Virus Infection Depends on Timing of Antigen Exposure in Mice

Yamamoto¹,

Suzuki²,

Suzuki³

et al. 2001

J Virol

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To study which phase of viral infection promotes antigen sensitization via the airway and which type of antigen-presenting cells contributes to antigen sensitization, BALB/c mice were sensitized by inhalation of ovalbumin (OA) during the acute phase or the recovery phase of influenza A virus infection, and then 3 weeks later animals were challenged with OA. The numbers of eosinophils and lymphocytes, the amounts of interleukin-4 (IL-4) and IL-5 in the bronchoalveolar lavage fluid, and the serum levels of OA-specific immunoglobulin G1 (IgG1) and IgE increased in mice sensitized during the acute phase (acute phase group), while a high level of gamma interferon production was detected in those sensitized during the recovery phase (recovery phase group). In the acute phase group, both major histocompatibility complex class II molecules and CD11c were strongly stained on the bronchial epithelium; in the recovery phase group, however, neither molecule was detected. OA-capturing dendritic cells (DCs) migrated to the regional lymph nodes, and a small number of OA-capturing macrophages were also observed in the lymph nodes of the acute phase group. In the recovery group, however, no OA-capturing DCs were detected in either the lungs or the lymph nodes, while OAcapturing macrophages were observed in the lymph nodes. These results indicate that the timing of antigen sensitization after viral infection determines the type of immune response.

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Section: Discussionmentioning

confidence: 99%

“…Clinically, respiratory virus infection has been proposed as a common triggering factor in the development of allergy in children (9,10,33). Schwarze et al showed that in mice, inhalation of an antigen after respiratory syncytial virus (RSV) infection increased both airway responsiveness and eosinophil influx to the lung (23).…”

mentioning

confidence: 99%

Immune Response Induced by Airway Sensitization after Influenza A Virus Infection Depends on Timing of Antigen Exposure in Mice

Yamamoto¹,

Suzuki²,

Suzuki³

et al. 2001

J Virol

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“…There may be at least two factors to explain this: age and genetic predisposition. It is most often children, particularly those with a family history of atopy, who develop chronic wheezing subsequent to acute bronchiolitis [20]. The correlation between virus IgE levels and the likelihood of developing wheezing [21] may reflect the predisposition to atopy in these patients.…”

Section: Consequences Of Antigen Challenge In Vitro and In Vivo In Unmentioning

confidence: 99%

Parainfluenza virus type-3 infection attenuates the respiratory effects of antigen challenge in sensitized guinea pigs

Kudlacz¹,

Knippenberg²

1995

Inflamm Res

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Respiratory viral infections not only exacerbate asthma symptoms but may also be important in the pathogenesis of the disease. We therefore explored the effects of respiratory viral infection on the respiratory response of sensitized guinea pigs to antigen challenge. Lung tissue obtained from uninfected guinea pigs sensitized to ovalbumin aerosol released histamine upon incubation with the antigen in vitro. After antigen challenge in vivo, sensitized animals had significantly greater numbers of eosinophils in their bronchoalveolar lavage fluid than did nonsensitized animals and exhibited airway hyperresponsiveness to methacholine aerosol. When ovalbumin sensitization was initiated 7 days after inoculation with parainfluenza virus type-3 (PI-3), antigen challenge elicited little histamine release from infected lung tissue in vitro. Likewise, subsequent to antigen challenge in vivo, animals failed to exhibit airway hyperresponsiveness or an increased eosinophil population in bronchoalveolar lavage fluid. Similar effects were observed when sensitization was begun 19 days after PI-3 virus inoculation. The mechanism(s) responsible for the attenuated responses to antigen in PI-3 infected animals are unknown but may involve virus-induced effects on immune cells.

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“…In some instances, follow up has been at a variable time interval since the illness and sometimes a control group has not been included.' 912 15 The findings have been contradictory on the role of atopy,' 4 14 1 -18 and have suggested that environmental factors such as family size,4 1319 parental smoking,' 9 18 20 21 breast feeding, '3 19 and neonatal respiratory illness'8 19 may be contributing to either the initial illness, subsequent symptoms, or both. There are also claims that bronchiolitis in infancy contributes to chronic airways obstruction in adult life.…”

mentioning

confidence: 99%

Respiratory status and allergy after bronchiolitis.

Murray

Webb

O’Callaghan

et al. 1992

Archives of Disease in Childhood

176

102

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As part of a long term prospective study, 73 children who had been admitted to hospital with viral bronchiolitis as infants, were reviewed 5-5 years later and compared with a carefully matched control group. In the postbronchiolitis group, there was a highly significant increase in respiratory symptoms including wheezing (42.5% v 15-0%, relative risk=2-8).Although atopy in the family was not significantly increased in the index group, personal atopy was more prevalent. However, personal atopy was not significantly more prevalent in the symptomatic postbronchiolitis, compared with those who were symptom free, and so did not account for the high prevalence of postbronchiolitis wheezing in this cohort. In addition, in a stepwise logistic regressional model, bronchiolitis remained a significant predictor of wheezing after adjusting for potential confounding variables, including atopy. Bronchial responsiveness to histamine was significantly increased in the index group. However, no significant relationship of positive tests to wheezing could be demonstrated, and a high rate of positive responses was noted in the controls.

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Patterns of allergic respiratory disease in children with a past history of bronchiolitis

Cited by 48 publications

References 13 publications

Immune Response Induced by Airway Sensitization after Influenza A Virus Infection Depends on Timing of Antigen Exposure in Mice

Immune Response Induced by Airway Sensitization after Influenza A Virus Infection Depends on Timing of Antigen Exposure in Mice

Parainfluenza virus type-3 infection attenuates the respiratory effects of antigen challenge in sensitized guinea pigs

Respiratory status and allergy after bronchiolitis.

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