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Comparison of innate immune responses towards rhinovirus infection of primary nasal and bronchial epithelial cells
Author(s) -
Alves Marco P.,
Schögler Aline,
Ebener Simone,
Vielle Nathalie J.,
Casaulta Carmen,
Jung Andreas,
Moeller Alexander,
Geiser Thomas,
Regamey Nicolas
Publication year - 2016
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1111/resp.12692
Subject(s) - rhinovirus , medicine , immunology , cytokine , viral replication , viral load , immune system , pathogenesis , proinflammatory cytokine , innate immune system , receptor , virology , inflammation , virus
Background and objective Rhinoviruses ( RV ) replicate in both upper and lower airway epithelial cells. We evaluated the possibility of using nasal epithelial cells ( NEC ) as surrogate of bronchial epithelial cells ( BEC ) for RV pathogenesis cell culture studies. Methods We used primary paired NEC and BEC cultures established from healthy subjects and compared the replication of RV belonging to the major ( RV 16) and minor ( RV1B ) group, and the cellular antiviral and proinflammatory cytokine responses towards these viruses. We related antiviral and pro‐inflammatory responses of NEC isolated from CF and COPD patients with those of BEC . Results RV 16 replication and major group surface receptor ( ICAM ‐1) expression were higher in healthy NEC compared with BEC ( P < 0.05); RV1B replication and minor group surface receptor ( LDLR ) expression were similar. Healthy NEC and BEC produced similar levels of IFN ‐β and IFN ‐λ2/3 upon RV infection or after simulation with poly( IC ). IL ‐8 production was similar between healthy NEC and BEC . IL ‐6 release at baseline ( P < 0.01) and upon infection with RV 16 ( P < 0.05) and poly( IC ) stimulation ( P < 0.05) was higher in NEC . RV1B viral load in NEC was related to RV1B viral load in BEC (r = 0.49, P = 0.01). There was a good correlation of IFN levels between NEC and BEC (r = 0.66, P = 0.0004 after RV1B infection). IL ‐8 production in NEC was related to IL ‐8 production in BEC (r = 0.48, P = 0.02 after RV1B infection). Conclusion NEC are a suitable alternative cellular system to BEC to study the pathophysiology of RV infections and particularly to investigate IFN responses induced by RV infection.