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Göteborgs universitets publikationer

Effects of Tobacco Smoke on IL-16 in CD8+ Cells from Human Airways and Blood: a Key Role for Oxygen Free Radicals?

Författare och institution:
Anders Andersson (Institutionen för medicin, avdelningen för invärtesmedicin); Apostolos Bossios (Krefting Research Centre); Carina Malmhäll (Krefting Research Centre); Margareta Sjöstrand (Krefting Research Centre); Maria Eldh (Krefting Research Centre); Britt-Marie Eldh (Institutionen för medicin, avdelningen för invärtesmedicin); Pernilla Glader (Institutionen för medicin, avdelningen för invärtesmedicin); Bengt Andersson (-); Ingemar Qvarfordt (Institutionen för medicin, avdelningen för invärtesmedicin); Gerdt C. Riise (Institutionen för medicin, avdelningen för invärtesmedicin); Anders Lindén (Institutionen för medicin, avdelningen för invärtesmedicin)
Publicerad i:
AJP - Lung cellular and molecular physiology, 300 ( 1 ) s. L43-L55
Artikel, refereegranskad vetenskaplig
Sammanfattning (abstract):
Chronic exposure to tobacco smoke leads to an increase in the frequency of infections and in CD8(+) and CD4(+)cells as well as the CD4(+) chemo-attractant cytokine IL-16 in the airways. Here, we investigated whether tobacco smoke depletes intracellular IL-16 protein and inhibits de novo production of IL-16 in CD8(+) cells from human airways and blood, while at the same time increasing extracellular IL-16 and whether oxygen free radicals (OFR) are involved. Intracellular IL-16 protein in CD8(+) cells and mRNA in all cells was decreased in bronchoalveolar lavage (BAL) samples from chronic smokers. This was also the case in human blood CD8(+) cells exposed to water-soluble tobacco smoke components in vitro; in which oxidized proteins were markedly increased. Extracellular IL-16 protein was increased in cell-free BAL fluid from chronic smokers and in human blood CD8(+) cells exposed to water-soluble tobacco smoke components in vitro. This was not observed in occasional smokers after short-term exposure to tobacco smoke. A marker of activation (CD69) was slightly increased whereas other markers of key cellular functions (membrane integrity, apoptosis and proliferation) in human blood CD8(+) cells in vitro were negatively affected by water-soluble tobacco smoke components. An OFR scavenger prevented these effects whereas a protein synthesis inhibitor, a beta-adrenoceptor, a glucocorticoid receptor agonist, a phosphodiesterase, a calcineurin phosphatase and a caspase-3 inhibitor did not. In conclusion, tobacco smoke depletes preformed intracellular IL-16 protein, inhibits its de novo synthesis and distorts key cellular functions in human CD8(+) cells. OFR may play a key role in this context.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
Medicinska grundvetenskaper ->
Mikrobiologi inom det medicinska området
Klinisk medicin ->
Dermatologi och venereologi
adaptive immunity, glucocorticoid, chronic obstructive pulmonary disease
Postens nummer:
Posten skapad:
2010-12-20 11:44
Posten ändrad:
2011-12-07 09:49

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