Azithromycin induces anti-viral effects in cultured bronchial epithelial cells from COPD patients

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift


Rhinovirus infection is a major cause of chronic obstructive pulmonary disease (COPD) exacerbations and may contribute to the development into severe stages of COPD. The macrolide antibiotic azithromycin may exert anti-viral actions and has been reported to reduce exacerbations in COPD. However, little is known about its anti-viral actions on bronchial epithelial cells at clinically relevant concentrations. Primary bronchial epithelial cells from COPD donors and healthy individuals were treated continuously with azithromycin starting 24 h before infection with rhinovirus RV16. Expression of interferons, RIG-I like helicases, pro-inflammatory cytokines and viral load were analysed. Azithromycin transiently increased expression of IFNβ and IFN? 1 and RIG-I like helicases in un-infected COPD cells. Further, azithromycin augmented RV16-induced expression of interferons and RIG-I like helicases in COPD cells but not in healthy epithelial cells. Azithromycin also decreased viral load. However, it only modestly altered RV16-induced pro-inflammatory cytokine expression. Adding budesonide did not reduce interferon-inducing effects of azithromycin. Possibly by inducing expression of RIG-I like helicases, azithromycin increased rhinovirus-induced expression of interferons in COPD but not in healthy bronchial epithelium. These effects would reduce bronchial viral load, supporting azithromycin's emerging role in prevention of exacerbations of COPD.


Enheter & grupper

Ämnesklassifikation (UKÄ) – OBLIGATORISK

  • Lungmedicin och allergi
TidskriftScientific Reports
StatusPublished - 2016 jun 28
Peer review utfördJa

Relaterad forskningsoutput

Mandy Menzel, 2018, Lund: Lund University, Faculty of Medicine. 76 s.

Forskningsoutput: AvhandlingDoktorsavhandling (sammanläggning)

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