Abstract
The susceptibility to respiratory syncytial virus (RSV) infection in early life has been associated with a deficient T-helper cell type 1 (Th1) response. Conversely, healthy adults generally do not exhibit severe illness from RSV infection. In the current study, we investigated whether Th1 cytokine IFN-γ is essential for protection against RSV and RSV-associated comorbidities in adult mice. We found that, distinct from influenza virus, prior RSV infection does not induce significant IFN-γ production and susceptibility to secondary Streptococcus pneumoniae infection in adult wild-type (WT) mice. In ovalbumin (OVA)-induced asthmatic mice, RSV super-infection increases airway neutrophil recruitment and inflammatory lung damage but has no significant effect on OVA-induced eosinophilia. Compared with WT controls, RSV infection of asthmatic Ifng−/− mice results in increased airway eosinophil accumulation. However, a comparable increase in eosinophilia was detected in house dust mite (HDM)-induced asthmatic Ifng−/− mice in the absence of RSV infection. Furthermore, neither WT nor Ifng−/− mice exhibit apparent eosinophil infiltration during RSV infection alone. Together, these findings indicate that, despite its critical role in limiting eosinophilic inflammation during asthma, IFN-γ is not essential for protection against RSV-induced exacerbation of asthmatic inflammation in adult mice.
Highlights
Asthma is the most common chronic disease in the world with more than 235 million people affected
S. pneumoniae infection in adult mice. In both ovalbumin (OVA) or house dust mite (HDM)induced asthmatic mice, we found that respiratory syncytial virus (RSV) infection induces neutrophil recruitment but has no significant impact on asthma-associated eosinophilia
It has been well established that influenza A virus (IAV) infection impairs innate antibacterial immunity and thereby increases susceptibility to secondary bacterial pneumonia
Summary
Asthma is the most common chronic disease in the world with more than 235 million people affected. In young children and immunocompromised patients, asthmatic disease is often complicated with common viral infections such as respiratory syncytial virus (RSV) [1,2,3,4,5]. While several studies have explored the causal role of a RSV infection in asthma development, wherein RSV infection occurs first, leading to lung development conducive for asthma, the mechanisms underlying the effect of RSV super-infection on augmentation of pre-existing asthma remains to be fully understood. RSV infection occurs at a high rate among children under the age of 5 and can lead to decreased effectiveness of asthma medications such as steroids [6,7,8]. Adults normally do not exhibit severe illness from an RSV infection and experience milder exacerbation in asthmatic disease. It has been suggested that a deficient T-helper cell type
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