Effect of Bovine Respiratory Syncytial Virus Infection on Hypersensitivity to Inhaled &lt;i&gt;Micropolyspora faeni&lt;/i&gt;

Gershwin, Laurel J.; Himes, S R; Dungworth, D. L.; Giri, Shri N.; Friebertshauser, Kathleen E.; Camacho, Marisabel Alvarez

doi:10.1159/000236712

Cited by 25 publications

(16 citation statements)

References 7 publications

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“…These studies and additional data from a rat model of influenza infection [28] and bovine model of RSV infection [29] demonstrate that viral lower respiratory tract infections can enhance allergic sensitization to inhaled antigens and prevent the development of tolerance which may be induced by allergen exposure via the airways in the absence of infection (table 1). Among the mechanisms involved, increased permeability of the airway mucosa to allergens and recruitment of dendritic cells to the airway epithelium during acute infection may be important, facilitating sensitization through increased antigen uptake and more effective antigen presentation.…”

Section: Parainfluenza Infection Results In Increased Mucosal Permeabmentioning

confidence: 93%

Respiratory viral infections as promoters of allergic sensitization and asthma in animal models

Schwarze¹,

Gelfand²

2002

Eur Respir J

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Respiratory viral infections as promoters of allergic sensitization and asthma in animal models. J. Schwarze, E.W. Gelfand. #ERS Journals Ltd 2002. ABSTRACT: Respiratory virus infections can trigger exacerbations of asthma and may also contribute to allergic sensitization to aeroallergens and the development of asthma. Conversely, atopy may predispose to more severe virus-induced airway disease. The animal models reviewed in this article support the hypothesis that respiratory virus infections can promote allergic sensitization and the development of asthma. Respiratory viruses can prevent induction of tolerance and enhance sensitization to inhaled allergens resulting in increased airway inflammation and airway hyperresponsiveness.Probable mechanisms involved in this enhanced sensitization are increased permeability of the airway mucosa to allergens and recruitment of dendritic cells to the respiratory epithelium during acute infection. Factors involved in augmenting the consequences of allergic airway sensitization appear to be T-cells, especially CD8z T-cells as regulators of this process, interleukin-5 as a pivotal cytokine for eosinophilic airway inflammation and eosinophils themselves as effector cells triggering airway hyperresponsiveness. Depending on the timing of allergen exposure, respiratory virus infections which elicit a significant type 1 T-helper cell cytokine response may also downregulate allergic sensitization.Respiratory virus infections in animals previously sensitized to aeroallergens result in prolonged increases in inflammation and airway responsiveness, indicating that critical interactions between immune responses to allergen sensitization and the responses to infection can lead to more severe disease.Taken together, animal models have proved valuable in generating a number of plausible pathogenetic concepts, and can be used to address a host of unresolved questions regarding the immunology of respiratory virus infections, allergic sensitization and asthma.

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Section: Parainfluenza Infection Results In Increased Mucosal Permeabmentioning

confidence: 93%

Respiratory viral infections as promoters of allergic sensitization and asthma in animal models

Schwarze¹,

Gelfand²

2002

Eur Respir J

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“…A conflicting study in a similar guinea pig model showed impaired airway sensitization after parainfluenza type III infection and the loss of airway hyperresponsiveness (30). In a bovine model, RSV infection enhanced sensitization to an inhaled antigen (31).…”

Section: Discussionmentioning

confidence: 99%

Respiratory syncytial virus infection results in airway hyperresponsiveness and enhanced airway sensitization to allergen.

Schwarze¹,

Hamelmann²,

Bradley³

et al. 1997

J. Clin. Invest.

311

242

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Viral respiratory infections can predispose to the development of asthma by mechanisms that are presently undetermined. Using a murine model of respiratory syncytial virus (RSV) infection, acute infection is associated with airway hyperresponsiveness as well as enhanced responses to subsequent sensitization to allergen. We demonstrate that acute viral infection results in increased airway responsiveness to inhaled methacholine and pulmonary neutrophilic and eosinophilic inflammation. This response is associated with predominant production of Th-1-type cytokines in peribronchial lymph node cells in vitro. Mice sensitized to ovalbumin via the airways after RSV infection developed increased airway responsiveness to methacholine and pulmonary eosinophilic and neutrophilic inflammation, associated with the predominant production of Th-2-type cytokines.

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“…RSV-infected murine lungs were characterized by increased eosinophilia, cytokine production (including IL-4), and inflammation, including up-regulation of adhesion molecules and chemokines. 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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Effect of Bovine Respiratory Syncytial Virus Infection on Hypersensitivity to Inhaled <i>Micropolyspora faeni</i>

Cited by 25 publications

References 7 publications

Respiratory viral infections as promoters of allergic sensitization and asthma in animal models

Respiratory viral infections as promoters of allergic sensitization and asthma in animal models

Respiratory syncytial virus infection results in airway hyperresponsiveness and enhanced airway sensitization to allergen.

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

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