The airway interferon landscape is altered in bronchiectasis and differs according to anatomical site

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Background: Viruses may be important exacerbation triggers in bronchiectasis, yet the key anti-viral mediators, Type-I and -III interferons (IFNs), are poorly characterised in this disease. We hypothesised that antiviral immunity would be altered in bronchiectasis. Methods: Soluble anti-viral mediators were measured within upper (nasosorption) and lower (bronchoalveolar lavage (BAL)) samples from 16 bronchiectasis and 33 healthy subjects via MSD immunoassay. To study the innate response to virus, bronchial epithelial cells were cultured from bronchiectasis and healthy subjects (n=3 per group) and infected ex vivo with rhinovirus (RV) A16. Results: Antiviral immune mediators in the lower airway were reduced in bronchiectasis compared to healthy subjects with significantly reduced BAL concentrations of the interferon-inducible protein CXCL11/I-TAC (P<0.001) and trends towards reduced concentrations of IFN-λ1 (P=0.062) and CXCL10/IP-10 (P=0.069). By contrast, nasal concentrations of the same mediators were either increased (CXCL11/I-TAC and CXCL10, both P=0.023) or no different (IFN-λ1) in bronchiectasis compared to healthy subjects. In line with MSD data, bronchial epithelial cells from bronchiectasis subjects had deficient IFNβ and IFNλ1 mRNA induction at 24- and 72-hours post RV infection (P<0.05). Our ongoing studies are evaluating responses of nasal epithelial cells from these subjects. Conclusions: Bronchiectasis is characterised by reduced antiviral immune mediators in the lower airways compared to healthy subjects with opposite effects seen in the upper airway. Dysregulated antiviral immunity could therefore underpin susceptibility to viral exacerbations in bronchiectasis.

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