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Systemic cytokine signaling via IL-17 in smokers with obstructive pulmonary disease: a link to bacterial colonization?

Artikel i vetenskaplig tidskrift
Författare Kristina Andelid
Sara Tengvall
Anders Andersson
B. Levanen
Karin Christenson
Pernilla Jirholt
Christina Åhrén
Ingemar Qvarfordt
Ann Ekberg-Jansson
Anders Lindén
Publicerad i International Journal of Chronic Obstructive Pulmonary Disease
Volym 10
Sidor 689-702
ISSN 1178-2005
Publiceringsår 2015
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Institutionen för medicin, avdelningen för invärtesmedicin och klinisk nutrition
Institutionen för biomedicin, avdelningen för infektionssjukdomar
Sidor 689-702
Språk en
Länkar dx.doi.org/10.2147/copd.s76273
Ämnesord COPD, exacerbation, infection, neutrophil, lung, opportunist, EUROPEAN-COMMUNITY, CHEMOKINE RELEASE, ENDOTHELIAL-CELLS, EPITHELIAL-CELLS, CIGARETTE-SMOKE, STABLE COPD, GRO-ALPHA, EXPRESSION, INFLAMMATION, INTERLEUKIN-8, Respiratory System
Ämneskategorier Klinisk medicin

Sammanfattning

We examined whether systemic cytokine signaling via interleukin (IL)-17 and growth-related oncogene-alpha (GRO-alpha) is impaired in smokers with obstructive pulmonary disease including chronic bronchitis (OPD-CB). We also examined how this systemic cytokine signaling relates to bacterial colonization in the airways of the smokers with OPD-CB. Currently smoking OPD-CB patients (n=60, corresponding to Global initiative for chronic Obstructive Lung Disease [ GOLD] stage I-IV) underwent recurrent blood and sputum sampling over 60 weeks, during stable conditions and at exacerbations. We characterized cytokine protein concentrations in blood and bacterial growth in sputum. Asymptomatic smokers (n=10) and never-smokers (n=10) were included as control groups. During stable clinical conditions, the protein concentrations of IL-17 and GRO-alpha were markedly lower among OPD-CB patients compared with never-smoker controls, whereas the asymptomatic smoker controls displayed intermediate concentrations. Notably, among OPD-CB patients, colonization by opportunistic pathogens was associated with markedly lower IL-17 and GRO-alpha, compared with colonization by common respiratory pathogens or oropharyngeal flora. During exacerbations in the OPD-CB patients, GRO-alpha and neutrophil concentrations were increased, whereas protein concentrations and messenger RNA for IL-17 were not detectable in a reproducible manner. In smokers with OPD-CB, systemic cytokine signaling via IL-17 and GRO-alpha is impaired and this alteration may be linked to colonization by opportunistic pathogens in the airways. Given the potential pathogenic and therapeutic implications, these findings deserve to be validated in new and larger patient cohorts.

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