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

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

Clin Exp Allergy. 2017 Dec 30;:

Authors: Jeon YJ, Lim JH, An S, Jo A, Han DH, Won TB, Kim DY, Rhee CS, Kim HJ

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 if higher loads of influenza A virus (IAV) in allergic nasal mucosa could be controlled with IFN treatment.
METHODS: IAV mRNA, viral titers 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 mouse, 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: IAV mRNA levels and viral titers were significantly higher in ARNE compared with NHNE cells. IFN-β and -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 titers in IAV-infected ARNE cells. In vivo AR mouse were exhibited higher viral load after IAV infection but intranasal inoculation of IFN-λ completely decreased IAV protein expression and viral titer 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. This article is protected by copyright. All rights reserved.

PMID: 29288502 [PubMed - as supplied by publisher]

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