Azithromycin induces anti-viral effects in cultured bronchial epithelial cells from COPD patients
(2016) In Scientific Reports 6.- Abstract
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... (More)
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.
(Less)
- author
- Menzel, Mandy LU ; Akbarshahi, Hamid LU ; Bjermer, Leif LU and Uller, Lena LU
- organization
- publishing date
- 2016-06-28
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Scientific Reports
- volume
- 6
- article number
- 28698
- publisher
- Nature Publishing Group
- external identifiers
-
- pmid:27350308
- wos:000378866400001
- scopus:84976413658
- ISSN
- 2045-2322
- DOI
- 10.1038/srep28698
- language
- English
- LU publication?
- yes
- id
- e1f3b82c-01d0-438f-8976-9180afef6182
- date added to LUP
- 2017-01-19 13:34:24
- date last changed
- 2025-01-25 21:38:12
@article{e1f3b82c-01d0-438f-8976-9180afef6182,
abstract = {{<p>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.</p>}},
author = {{Menzel, Mandy and Akbarshahi, Hamid and Bjermer, Leif and Uller, Lena}},
issn = {{2045-2322}},
language = {{eng}},
month = {{06}},
publisher = {{Nature Publishing Group}},
series = {{Scientific Reports}},
title = {{Azithromycin induces anti-viral effects in cultured bronchial epithelial cells from COPD patients}},
url = {{http://dx.doi.org/10.1038/srep28698}},
doi = {{10.1038/srep28698}},
volume = {{6}},
year = {{2016}},
}