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Review
. 2014 Sep;96(3):391-6.
doi: 10.1189/jlb.3RI0314-129R. Epub 2014 Jun 5.

Respiratory viral infection, epithelial cytokines, and innate lymphoid cells in asthma exacerbations

Rakesh K Kumar  1 , Paul S Foster  2 , Helene F Rosenberg  3
Affiliations
Review

Respiratory viral infection, epithelial cytokines, and innate lymphoid cells in asthma exacerbations

Rakesh K Kumar et al. J Leukoc Biol. 2014 Sep.

Abstract

Exacerbations of asthma are most commonly triggered by viral infections, which amplify allergic inflammation. Cytokines released by virus-infected AECs may be important in driving this response. This review focuses on accumulating evidence in support of a role for epithelial cytokines, including IL-33, IL-25, and TSLP, as well as their targets, type 2 innate lymphoid cells (ILC2s), in the pathogenesis of virus-induced asthma exacerbations. Production and release of these cytokines lead to recruitment and activation of ILC2s, which secrete mediators, including IL-5 and IL-13, which augment allergic inflammation. However, little information is currently available about the induction of these responses by the respiratory viruses that are strongly associated with exacerbations of asthma, such as rhinoviruses. Further human studies, as well as improved animal experimental models, are needed to investigate appropriately the pathogenetic mechanisms in virus-induced exacerbations of asthma, including the role of ILCs.

Keywords: Th2; allergy; animal models; interleukin-33.

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Figures

Figure 1.
Figure 1.. Infection of respiratory epithelial cells elicits inflammation via the activation of ILC2s.
Respiratory viruses interact with one or more PRRs, replicate within, and are released from AECs, with resultant cellular injury. This is likely to lead to release of the Th2-promoting cytokines IL-33, IL-25, and TSLP, in turn recruiting ILC2s, which amplify inflammation (via release of IL-5 and IL-13) and promote airway repair/fibrosis (via amphiregulin, IL-13, and arginase-1). Although IL-33 has been detected in the airways in response to primary infection with influenza and PVM [62, 63] and specifically from alveolar macrophages in response to influenza [64], the links among viral infection, release of Th2-promoting cytokines from epithelial cells, and exacerbation of allergic asthmatic inflammation remain to be explored.
See this image and copyright information in PMC

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