Rhinovirus infection in murine chronic allergic rhinosinusitis model

Abstract

We successfully established a mouse model of upper airway RV infection by nasal inoculation with RV1B. Although there was histologically-proven increased RV infection in the CARS model, the infection did not intensify sinonasal inflammation.

Lung epithelial cells have virus-specific and shared gene expression responses to infection by diverse respiratory viruses

“…Alternatively, the reduced response to MHV by epithelial cells may reflect the different cellular tropism of MHV. In contrast to PR8 and RV, which are known to infect epithelial cells in the murine respiratory tract, MHV-1 has only been reported in alveolar macrophages [2,6,12].…”

“…The signature genes up-regulated by RV included kallikrein-1 and ten kallikrein-1-related peptidases and additional proteins involved in tissue remodeling (S4 Table). Although tissue remodeling is not likely to be relevant in murine models of rhinovirus infection alone, due to the limited damage, it may be an important factor in murine models of rhinovirus-induced allergic asthma [1,2,41]. Rhinovirus infections are a significant cause of asthma exacerbations, which correspond with inflammatory responses in the airways.…”

“…Minor group rhinoviruses, including RV1B, use low-density lipoprotein receptor to enter either human or murine cells. Because RV1B can replicate in mouse cells, it has been used to study immune responses and mechanisms of asthma exacerbation in infected mice [1][2][3][4][5]. Intranasal inoculation of mice with a high dose of RV1B results in viral replication and an early inflammatory response in the respiratory tract without clinical signs of disease [1,[3][4][5].…”

“…Intranasal inoculation of mice with a high dose of RV1B results in viral replication and an early inflammatory response in the respiratory tract without clinical signs of disease [1,[3][4][5]. RV1B antigens have been detected in cells of the epithelia and lamina propria of the upper respiratory tract of infected mice [2,4].…”

In vivo experimental models of infection and disease

“…A mouse model of chronic allergic rhinosinusitis was induced by 5 weeks of repetitive nasal OVA challenges. 194 Increased RV-A1 yields were reported in the nasal tissue of mice with rhinosinusitis, although inflammatory cytokine production and histopathology were unaffected. 194 This study served to illustrate the range of additional diseases where RV infection has been shown to be relevant in human populations where animal models are available for future research (e.g., cystic fibrosis).…”