Immunoglobulin E Responses and Lung Pathology Resulting from Aerosol Exposure of Calves to Respiratory Syncytial Virus and &lt;i&gt;Micropolyspora faeni&lt;/i&gt;

Gershwin, Laurel J.; Dungworth, D. L.; Himes, S R; Friebertshauser, Kathleen E.

doi:10.1159/000235192

Cited by 30 publications

(13 citation statements)

References 9 publications

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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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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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“…In a previous study we examined the effect of BRSV infection on aerosol exposure of naive and Micropolysporafaeni (Mf)-sensitized calves. We reported that the in halation of Mf during BRSV infection of previously Mf aerosol-sensitized calves enhanced virus-specific IgE pro duction and severity of pulmonary disease expression [10].…”

Section: Introductionmentioning

confidence: 90%

Effect of Bovine Respiratory Syncytial Virus Infection on Hypersensitivity to Inhaled <i>Micropolyspora faeni</i>

Gershwin

Himes

Dungworth

et al. 1994

Int Arch Allergy Immunol

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Respiratory syncytial virus causes mild-to-severe respiratory disease in human infants and young children; a closely related bovine respiratory syncytial virus causes a similar disease pattern in calves. Increased disease severity in atopic children suggests that allergic reactivity may enhance the severity of RSV-induced disease. To examine the association between bovine respiratory syncytial virus (BRSV) infection and allergic reactivity two groups of calves were exposed to aerosolized Micropolyspora faeni (Mf) during an experimental BRSV infection. One group exposed to Mf concurrent with BRSV was challenge-exposed to Mf while infected a second time with BRSV, while the other similarly sensitized and infected group was mock challenged. A control group was exposed only to Mf aerosol and another control group was infected with virus but not exposed to Mf aerosol. Parameters examined included: clinical signs, Mf-specific IgG and IgE, BRSV-specific antibody and IgE, leukotrienes C₄ and B₄ prostaglandins E₂, F_2α and D₂, and lung pathology. While the initial BRSV infection failed to enhance sensitization to inhaled Mf a second BRSV infection excerbated cinical signs resulting from Mf aerosol. Consideration of eicosanoid and antibody profiles together with clinical signs suggests that mechanisms of both type I and type III hypersensitivity were operative during Mf challenge of sensitized calves.

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“…Some have shown that RSV bronchiolitis is more severe in the first case. In several experimental systems, allergen sensitization preceded infection by several weeks and then challenge took place during RSV infection (Gershwin et al, 1990;Gershwin and Giri, 1992;Barends et al, 2002;Lambert et al, 2003). These experimental systems employed allergens such as Micropolyspora faeni (currently known as Saccharopolyspora rectivirgula), Ovalbumin (OVA), or carbon black.…”

Section: Mechanisms Of Allergen Induced Rsv Immunomodulationmentioning

confidence: 99%

Progress in Defining the Role of RSV in Allergy and Asthma: From Clinical Observations to Animal Models

Kalina

Gershwin

2004

Journal of Immunology Research

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Respiratory syncytial virus (RSV), an RNA virus in the family Paramyxoviridae, causes respiratory disease in humans. A closely related bovine RSV is responsible for a remarkably similar disease syndrome in young cattle. Severe RSV disease is characterized by bronchiolitis. The impact of RSV on human health is demonstrated annually when infants are admitted to the hospital in large numbers. Nearly every child will have been infected with RSV by the age of 3 years. While the disease is most severe in young infants and elderly people, it can re-infect adults causing mild upper respiratory tract disease throughout life. In addition, there is growing evidence that RSV infection may also predispose some children to the development of asthma. This is based on the observation that children who wheeze with RSV-induced bronchiolitis are more likely to develop into allergic asthmatics. Recent studies describe attempts to create an RSV induced asthma model in mice and other species; these have shown some degree of success. Such reports of case studies and animal models have suggested a wide range of factors possibly contributing to RSV induced asthma, these include timing of RSV infection with respect to allergen exposure, prior allergic sensitization, environmental conditions, exposure to endotoxin, and the genetic background of the person or animal. Herein, we primarily focus on the influence of RSV infection and inhalation of extraneous substances (such as allergens or endotoxin) on development of allergic asthma.

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Immunoglobulin E Responses and Lung Pathology Resulting from Aerosol Exposure of Calves to Respiratory Syncytial Virus and <i>Micropolyspora faeni</i>

Cited by 30 publications

References 9 publications

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

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

Effect of Bovine Respiratory Syncytial Virus Infection on Hypersensitivity to Inhaled <i>Micropolyspora faeni</i>

Progress in Defining the Role of RSV in Allergy and Asthma: From Clinical Observations to Animal Models

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