, Volume 20, Issue 2, pp 123-137

Changes of fatty acid composition and oxidative metabolism of human neutrophils migrating into an inflammatory exudate

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access


The peripheral blood neutrophils and the neutrophils accumulated into a skin-window experimental exudate were compared for their ability to release superoxide anion (O 2 ) and for their fatty acid composition, determined by capillary gaschromatography. The basal O 2 release and the phorbol myristate acetate (PMA)-induced O 2 release were not significantly different in the two neutrophil populations, while in response to formyl-methionyl-leucyl-phenylalanine (fMLP) the exudate cells showed an activity that was two fold higher than that of blood cells. The most significant changes of fatty acid composition of exudate versus blood cells were the following: i) increase of C16∶0 (palmitic acid) from 21.3±1.2% to 23.5±1.3% (+ 10.2%) of total fatty acids (p<0.001), ii) increase of C18:2 (linoleic acid) from 9.3±1.7% to 11.0±2.1% (+18.3%) (p=0.005), iii) decrease of C20∶4 (arachidonic acid) from 12.8±1.6% to 10.6±1.2% (−17.3%) (p<0.001), whereas C18∶1 (oleic acid) did not change. The total content of saturated or unsaturated fatty acids did not change. In exudate cells, a strong negative correlation was found between palmitic acid content and O 2 release in response to both fMLP and PMA (r=-0.52,p< 0.02 andr=−0.49,p<0.05, respectively) whereas arachidonic acid correlated positively, but weakly, with O 2 (r=0.40,p=0.07 andr=0.47,p=0.05, with fMLP and PMA as stimulants respectively). A positive correlation was also found between the arachidonic acid content of blood cells and the number of cells that migrated into the inflammatory exudate. These results indicate that the process of extravasation from blood into the exudate causes specific and consistent modifications of the fatty acid composition of neutrophils and suggest that these modifications have a role in the activation and the regulation of the O 2 forming system.