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. 2018 Mar;48(3):253-265.
doi: 10.1111/cea.13082. Epub 2018 Feb 1.

Type III interferons are critical host factors that determine susceptibility to Influenza A viral infection in allergic nasal mucosa

Y J Jeon  1 , J H Lim  1 , S An  2 , A Jo  2 , D H Han  1   2 , T-B Won  1   2 , D-Y Kim  1   2 , C-S Rhee  1   2 , H J Kim  1   2
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Type III interferons are critical host factors that determine susceptibility to Influenza A viral infection in allergic nasal mucosa

Y J Jeon et al. Clin Exp Allergy. 2018 Mar.

Abstract

Background: Allergic respiratory conditions have been associated with increased susceptibility to viral infection due to impaired interferon (IFN)-related immune responses, but the mechanisms for reinforcement of mucosal immunity against viral infection in allergic diseases are largely unknown.

Objectives: To determine whether IFN induction would be impaired in allergic nasal mucosa and to identify whether higher loads of influenza A virus (IAV) in allergic nasal mucosa could be controlled with IFN treatment.

Methods: Influenza A virus mRNA, viral titres and IFN expression were compared in IAV-infected normal human nasal epithelial (NHNE, N = 10) and allergic rhinitis nasal epithelial (ARNE, N = 10) cells. We used in vivo model of allergic rhinitis (BALB/c mice, N = 10) and human nasal mucosa from healthy volunteers (N = 72) and allergic rhinitis patients (N = 29) to assess the induction of IFNs after IAV infection.

Results: Influenza A virus mRNA levels and viral titres were significantly higher in ARNE compared with NHNE cells. IFN-β and IFN-λs were induced in NHNE and ARNE cells up to 3 days after IAV infection. Interestingly, induction of IFN-λs mRNA levels and the amount of secreted proteins were considerably lower in ARNE cells. The mean IFN-λs mRNA level was also significantly lower in the nasal mucosa of AR patients, and we found that recombinant IFN-λ treatment attenuated viral mRNA levels and viral titres in IAV-infected ARNE cells. In vivoAR mouse exhibited higher viral load after IAV infection, but intranasal inoculation of IFN-λ completely decreased IAV protein expression and viral titre in nasal mucosa of IAV-infected AR mouse.

Conclusion: Higher susceptibility of the allergic nasal mucosa to IAV may depend on impairment of type III IFN induction, and type III IFN is a key mechanistic link between higher viral loads and control of IAV infection in allergic nasal mucosa.

Keywords: allergic rhinitis; influenza A virus; nasal mucosa; type III interferon.

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