Neutrophil unsaturated fatty acid release by GM-CSF is impaired in cystic fibrosis

Lipids in Health and Disease

Short Paper

Serena Quattrucci¹  Sara Benedetti Valentini¹  Elena Bravo²  Mariarosaria Napolitano² 

[1] Centro Fibrosi Cistica di Riferimento Regione Lazio - Department of Pediatrics -University "La Sapienza", Viale Regina Elena, 324 - 00161, Roma, Italy;Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Viale Regina Elena, 199 - 00161, Roma, Italy;

关键词: Cystic Fibrosis;    Arachidonic Acid;    Cystic Fibrosis Transmembrane Conductance Regulator;    Cystic Fibrosis Patient;    Arachidonic Acid Release;   

DOI  :  10.1186/1476-511X-9-129

 received in 2010-09-30, accepted in 2010-11-08,  发布年份 2010

来源: Springer

【 摘 要 】

Dysregulated inflammation in cystic fibrosis (CF) is attributed to an altered production of inflammatory mediators derived from polyunsaturated lipids. In comparison to the arachidonic acid (AA) cascade, little is known about the modulation of docosahexaenoic acid (DHA) membrane release. We compared data on neutrophil DHA- and AA- release from both control (CT) and patients with CF using [3H]AA or [14C]DHA as a markers for, respectively, AA and DHA- release. Granulocyte-macrophage-colony stimulating factor stimulated DHA release from CT, but not CF, neutrophils. Comparison showed that both [14C]DHA and [3H]AA liberated after stimulation was higher in CT than in CF neutrophils. Since bioactive mediators derived from DHA are resolving factors and those derived from AA are both pro- and anti- inflammatory, these results suggest that CF is associated with a reduction of the release of PUFA-precursors of lipooxygenated resolving mediators. This leads to the hypothesis that defects in the resolving factors production could contribute to the inflammatory dysregulated processes in CF. Furthermore, the methodology used may help to improve knowledge on the regulation and resolution of inflammation.

【 授权许可】

CC BY   
© Bravo et al; licensee BioMed Central Ltd. 2010