Linoleic acid-deficient rat neutrophils show decreased bactericidal capacity, superoxide formation and membrane depolarization.

Essential fatty acid deficiency (EFAD) is associated with depressed inflammatory responses, e.g. neutrophil chemotaxis, which may be related to reduced generation of the arachidonate metabolite LTB4, a potent mediator for neutrophil activation. In this study we show that neutrophils from EFAD rats exhibited impairments of membrane depolarization and superoxide anion formation upon stimulation with a formylpeptide, FMLP, or when challenged with living Staphylococcus aureus (but not when activated with phorbol myristate acetate). Likewise, bactericidal capacity for S. aureus was depressed. However, ionomycin and FMLP stimulated intracellular Ca2+ elevations, phagocytic capacity, and conformational alterations as well as spreading were similar to control neutrophils. Thus, EFAD confers discrete functional abberations in neutrophils likely to be due to perturbation of arachidonate metabolism and/or membrane function.