Naslov
Chronic activation of polymorphonuclear leukocytes in COPD patients

Autori
Somborac Bačura, Anita ; Popović-Grle, Sanja ; Zovko, Vlasta ; Žanić Grubišić, Tihana

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
ERS Research Seminar: ''Proteases at the cutting edge: friends or foes in chronic lung diseases?'' / Borensztajn, Keren ; Taggart, Clifford - : European Respiratory Society, 2015, X-x

Skup
ERS Research Seminar: ''Proteases at the cutting edge: friends or foes in chronic lung diseases?''

Mjesto i datum
Amsterdam, Nizozemska, 11.11.2015. - 13.11.2015

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
chronic obstructive pulmonary disease ; cigarette smoke extract ; matrix metalloproteinase-9 ; poymorphonuclear leukocytes

Sažetak
Background: Cigarette smoking is a major risk factor for chronic obstructive pulmonary disease (COPD). Exposure to cigarette smoke and subsequent inflammatory response may cause a secretion of cellular proteases involved in a degradation of extracellular matrix in lungs. Objective: The aim of this study was to evaluate the difference in release of matrix metalloproteinase-9 (MMP-9) from polymorphonuclear leukocytes (PMN) between patients with COPD and healthy controls. Materials and Methods: The study included 23 patients with stable COPD and 9 healthy controls. PMN were isolated from blood of all participants and exposed to 4 % cigarette smoke extract (CSE) or basal culture media (as a control). After 20 h incubation, MMP-9 concentration and LDH activity were measured in PMN culture media using the ELISA and spectrophotometric method, respectively. Statistical analysis was performed using the SigmaStat program. Results: Exposure of PMN to 4 % CSE during 20 h incubation did not cause changes in LDH activity in PMN culture media comparing to untreated PMN (P=0.689), showing no toxic effects of CSE towards PMN under these conditions. In basal conditions when no stimulation was applied, PMN of COPD patients released significantly more MMP-9 compared with PMN of healthy controls (P=0.016). Stimulation of PMN of healthy controls with CSE increased the release of MMP-9 into the culture media (P=0.025), while no further increase over the high basal secretion rate was found in COPD patients. Conclusions: Results are showing chronic activation of PMN in patients with COPD and suggesting their indirect role in the degradation of extracellular matrix in lungs.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti, Farmacija

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