Abstract
The airway epithelium is the primary target of respiratory syncytial virus infection. It is an important component of the antiviral immune response. It contributes to the recruitment and activation of innate immune cells from the periphery through the secretion of cytokines and chemokines. This paper provides a broad review of the cytokines and chemokines secreted from human airway epithelial cell models during respiratory syncytial virus (RSV) infection based on a comprehensive literature review. Epithelium-derived chemokines constitute most inflammatory mediators secreted from the epithelium during RSV infection. This suggests chemo-attraction of peripheral immune cells, such as monocytes, neutrophils, eosinophils, and natural killer cells as a key function of the epithelium. The reports of epithelium-derived cytokines are limited. Recent research has started to identify novel cytokines, the functions of which remain largely unknown in the wider context of the RSV immune response. It is argued that the correct choice of in vitro models used for investigations of epithelial immune functions during RSV infection could facilitate greater progress in this field.
Highlights
Respiratory syncytial virus (RSV) is a major respiratory pathogen and has been estimated to cause 64 million cases of respiratory disease each year [1]
This paper reviewed the importance of the airway epithelium in the control of innate immune responses to RSV infection, with a particular emphasis on the recruitment of peripheral immune cells
The secretion of more than 20 inflammatory mediators during RSV infection indicated that the airway epithelium contributes to the control of the local immune response
Summary
Respiratory syncytial virus (RSV) is a major respiratory pathogen and has been estimated to cause 64 million cases of respiratory disease each year [1]. The evidence suggests that RSV infection does not induce the extensive epithelial cytopathology observed in severe LRTIs [5,6,7,8]. The observed tissue damage was hypothesized to be immune cell-mediated [6]. The airway epithelium is the primary target of RSV infection and has been implicated as a frontline defense system against respiratory viruses [12]. It is an immunological barrier that elicits inflammatory responses when appropriate [12]. Respiratory viruses, such as RSV, are known to modulate epithelial defenses, such as the physical barrier and ciliated cell function, sensor functions, and the secretion of inflammatory mediators to facilitate the infection of the airways. The authors have focused on studies demonstrating secretion of inflammatory mediators following RSV infection in vitro in correlation with in vivo data
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