<b>Introduction:</b> A dysregulation between pro-inflammatory and pro-resolution mediators has been proposed as a potential contributor to chronic persistent inflammation in bronchiectasis. <b>Aim:</b> The aim of this study was to characterise lipids in the blood and airways in clinically stable bronchiectasis patients. <b>Methods:</b> 6 healthy volunteers, 10 mild, 15 moderate and 9 with severe bronchiectasis were recruited whilst clinically stable. All participants had blood taken and underwent bronchoscopy [bronchoalveolar lavage (BAL) and brushings obtained]. Lipids were measured by liquid chromatography and mass spectrometry and transcription of lipoxin A4 biosynthetic enzymes [5 Lipoxygenase(LOX), LTA4 hydrolase, 15LOX-A and 15LOX-B] was assessed by qRT-PCR. The AA metabolite lipids assessed were: anti-inflammmatory and pro-resolution Lipoxin A4, and the generally classified pro-inflammatory mediators Prostaglandin (PG)E2, 5 hydroxyeicosatetraenoic acid (5-HETE), 15 hydroxyeicosatetraenoic acid (15-HETE), Leukotriene (LT)B4 and 9-hydroxyoctadecadienoic acid (9-HODE). <b>Results:</b> In serum, there were significantly lower levels of Lipoxin A4 and higher levels of PGE2, 15HETE and LTB4 in moderate/severe disease compared to healthy controls, p=0.04, p=0.03, p=0.03 and p=0.02 respectively. In BAL, significantly higher levels of PGE2, 5-HETE, 15-HETE, 9 HODE and LTB4 in moderate/severe disease compared to healthy donors, p<0.0001, p=0.004, p=0.005, p=0.04 and p<0.0001 respectively. LTA4 hydrolase was the most abundantly expressed RNA in bronchial brushings, and 15LOX-B the least abundant gene. <b>Conclusion:</b> Dysregulation of LXA4 biosynthetic genes shift the balance to a pro-inflammatory mediator profile contributing towards persistent inflammation.
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