Peripheral blood cytokine responses and disease severity in respiratory syncytial virus bronchiolitis

Bont, Louis; Heijnen, Cobi J.; Kavelaars, Annemieke; Aalderen, W. M. C. van; Brus, F; Draaisma, Jos M. Th.; Geelen, Stefan M. van; Vught, H. J. Van; Kimpen, Jan L. L.

doi:10.1034/j.1399-3003.1999.14a24.x

Cited by 128 publications

(100 citation statements)

References 34 publications

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“…Several clinical studies have indicated a correlation of decreased IL-12 with severe cases of RSV-induced airway disease (46,55,56). These findings, along with a number of animal studies in allergy/asthma, suggest that this cytokine axis may play a significant role in determining the overall direction of the pulmonary response.…”

Section: Discussionmentioning

confidence: 70%

IL-13-Induced Airway Hyperreactivity During Respiratory Syncytial Virus Infection Is STAT6 Dependent

Tekkanat

Maassab

Cho

et al. 2001

The Journal of Immunology

130

109

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Airway damage and hyperreactivity induced during respiratory syncytial virus (RSV) infection can have a prolonged effect in infants and young children. These infections can alter the long-term function of the lung and may lead to severe asthma-like responses. In these studies, the role of IL-13 in inducing and maintaining a prolonged airway hyperreactivity response was examined using a mouse model of primary RSV infection. Using this model, there was evidence of significant airway epithelial cell damage and sloughing, along with mucus production. The airway hyperreactivity response was significantly increased by 8 days postinfection, peaked during days 10–12, and began to resolve by day 14. When the local production of Th1- and Th2-associated cytokines was examined, there was a significant increase, primarily in IL-13, as the viral response progressed. Treatment of RSV-infected mice with anti-IL-13 substantially inhibited airway hyperreactivity. Anti-IL-4 treatment had no effect on the RSV-induced responses. Interestingly, when IL-13 was neutralized, an early increase in IL-12 production was observed within the lungs, as was a significantly lower level of viral Ags, suggesting that IL-13 may be regulating an important antiviral pathway. The examination of RSV-induced airway hyperreactivity in STAT6−/− mice demonstrated a significant attenuation of the response, similar to the anti-IL-13 treatment. In addition, STAT6−/− mice had a significant alteration of mucus-producing cells in the airway. Altogether, these studies suggest that a primary factor leading to chronic RSV-induced airway dysfunction may be the inappropriate production of IL-13.

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Section: Discussionmentioning

confidence: 70%

IL-13-Induced Airway Hyperreactivity During Respiratory Syncytial Virus Infection Is STAT6 Dependent

Tekkanat

Maassab

Cho

et al. 2001

The Journal of Immunology

130

109

View full text Add to dashboard Cite

show abstract

“…However, the Th1/Th2 balance, as explanatory model for the pathogenesis of the RSV infection, is not absolute and has been contradicted by several human studies in which a Th2 predominance (21)(22)(23)(24)(25) and/or a decreased Th1 response (22,23,25) were not confirmed, implying that different mechanisms are involved in the immune-mediated events during severe RSV bronchiolitis.…”

Section: Th1 Cells Th2 Cells and Rsvmentioning

confidence: 97%

The role of Th17 and Treg responses in the pathogenesis of RSV infection

et al. 2015

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“…Additionally, in a bovine model RSV infection has been shown to enhance sensitization to subsequent airway Ag (61,62). Although still controversial, a variety of studies suggest that individuals who suffered an RSV infection during childhood are significantly predisposed to develop allergy and atopy either during early adulthood or later (63)(64)(65)(66)(67)(68)(69)(70).…”

Section: Discussionmentioning

confidence: 99%

Modulation of Inhaled Antigen-Induced IgE Tolerance by Ongoing Th2 Responses in the Lung

Hurst

Seymour

Muchamuel

et al. 2001

The Journal of Immunology

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The normal response to inhaled Ag is the absence of Ag-specific IgE and cytokine production to later Ag challenges. Although the mechanism of this aerosol-induced IgE tolerance is not completely understood, it may prevent sensitization to inhaled Ags, which could otherwise lead to allergy and asthma. We examined the consequences of ongoing Th1 and Th2 responses in the lungs of mice during OVA inhalation to mimic conditions that may subvert tolerance and lead to sensitization. We found that concurrent, secondary Th2 lung responses to keyhole limpet hemocyanin or primary responses to Nippostrongylus larvae or Asperigillus fumagatus extract prevented establishment of IgE tolerance to aerosolized OVA. Intranasal rIL-4 given before OVA aerosolization also prevented establishment of tolerance, whereas concurrent Th1 responses to influenza virus or Mycobacterium bovis bacillus Calmette-Guérin had no effect. However, once established, aerosol tolerance to OVA could not be completely broken by OVA rechallenge concurrent with a secondary Th2 response to keyhole limpet hemocyanin or A. fumagatus extract, or by intranasal rIL-4. These data suggest that the immune status of the lung of an individual may profoundly influence the initial response to inhaled Ag, and that aerosol-induced IgE tolerance may not be appropriately established in individuals undergoing concurrent, Th2-mediated responses to Ags or pathogens.

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Peripheral blood cytokine responses and disease severity in respiratory syncytial virus bronchiolitis

Cited by 128 publications

References 34 publications

IL-13-Induced Airway Hyperreactivity During Respiratory Syncytial Virus Infection Is STAT6 Dependent

IL-13-Induced Airway Hyperreactivity During Respiratory Syncytial Virus Infection Is STAT6 Dependent

The role of Th17 and Treg responses in the pathogenesis of RSV infection

Modulation of Inhaled Antigen-Induced IgE Tolerance by Ongoing Th2 Responses in the Lung

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