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Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
RSV Infection in Neonatal Mice Induces Pulmonary Eosinophilia Responsible for Asthmatic Reaction
Dan Zhang1,2,3, Jie Yang2, Yuanhui Zhao2,4
1State Key Laboratory of Pharmaceutical Biotechnology, Medical School, Nanjing University, Nanjing, China.
Insights
Early-life respiratory syncytial virus (RSV) infection exacerbates allergic asthma by promoting eosinophil activity. These eosinophils worsen lung inflammation and asthma symptoms, highlighting their role in post-infection allergic responses.
Area of Science:
- Immunology
- Pediatric Respiratory Medicine
- Allergy and Asthma Research
Background:
- Respiratory syncytial virus (RSV) is a major cause of infant respiratory infections and a risk factor for childhood asthma.
- Eosinophilic airway inflammation is a key feature of pediatric asthma, but the precise role of eosinophils in virus-induced asthma remains unclear.
Purpose of the Study:
- To investigate the role of pulmonary eosinophils in exacerbating allergic asthma following early-life respiratory syncytial virus (RSV) infection.
- To elucidate the mechanisms by which RSV-induced eosinophilia contributes to allergic respiratory inflammation and asthma development.
Main Methods:
- Neonatal mouse model of RSV infection followed by allergen challenge.
- Analysis of immune cell populations (eosinophils, ILC2, CD4+ T cells, macrophages) in the lungs.
- Adoptive transfer of eosinophils from infected mice into naive recipients.
- Assessment of asthma phenotypes (airway hyperresponsiveness, inflammation, mucus production).
- Evaluation of antigen presentation molecule expression on eosinophils.
Main Results:
- RSV infection in neonatal mice led to eosinophilia and exacerbated allergic asthma responses upon allergen stimulation.
- Adoptive transfer of eosinophils from RSV-infected mice worsened allergic lung inflammation and asthma symptoms in naive mice.
- RSV-infected eosinophils showed increased expression of CD80, CD86, and MHC II, promoting CD4+ T cell accumulation.
- Treatment with indomethacin attenuated the lung pathology induced by eosinophil transfer.
Conclusions:
- Pulmonary eosinophils play a significant role in mediating the proinflammatory responses that link early-life RSV infection to allergic asthma.
- RSV infection primes eosinophils to enhance antigen presentation and promote T cell responses, contributing to severe allergic airway disease.
- Targeting eosinophil-mediated inflammation may be a therapeutic strategy for preventing or treating asthma associated with early-life viral infections.
Abstract:
Respiratory syncytial virus (RSV) is a leading cause of lower respiratory tract infections in infants and young children. Severe respiratory viral infection in early life is intimately associated with childhood recurrent wheezing and is a risk factor for asthma later in life. Although eosinophilic airway inflammation is an important trait in asthma of children, the roles of pulmonary eosinophils in the disease have been inadequately understood. Here, we show that RSV infection in neonatal mice causes eosinophilia after allergen stimulation. We showed that RSV infection in neonatal mice exacerbated allergic asthma to allergen stimulation that was accompanied with increased detection of eosinophils in the lungs. In addition, we also detected accumulation of ILC2, CD4+ T cells, and macrophages. Importantly, adoptive transfer of eosinophils from asthmatic mice with early-life RSV infection exacerbated pulmonary pathologies associated with allergic respiratory inflammation in naive mice in response to foreign antigen. The induction of asthmatic symptoms including AHR, tracheal wall thickening, and mucus production became more severe after further stimulation in those mice. The expression of antigen presentation-related molecules like CD80, CD86, and especially MHC II was markedly induced in eosinophils from OVA-stimulated asthmatic mice. The accumulation of CD4+ T cells in the lungs was also significantly increased as a result of adoptive transfer of eosinophils. Importantly, the deterioration of lung pathology caused by adoptive transfer could be effectively attenuated by treatment with indomethacin, a nonsteroidal anti-inflammatory drug. Our findings highlight the significance of eosinophil-mediated proinflammatory response in allergic disease associated with early-life infection of the respiratory tract.
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