Premium
Prostaglandin and fatty acid modulation of Escherichia coli O157 phagocytosis by human monocytic cells
Author(s) -
Davidson J.,
Kerr A.,
Guy K.,
Rotondo D.
Publication year - 1998
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1998.00511.x
Subject(s) - phagocytosis , lipopolysaccharide , arachidonic acid , prostaglandin e2 , biology , extracellular , prostaglandin , prostaglandin e , monocyte , biochemistry , microbiology and biotechnology , chemistry , endocrinology , immunology , enzyme
Phagocytosis by human monocytes is an important primary survival mechanism particularly during bacterial infection. However, the processes that control the events and mediators involved in the activation of monocytes and their impact on the phagocytosis of bacteria are poorly understood. The effect of bacterial endotoxin, interleukin‐1β (IL‐1β), fatty acids and prostaglandin E 2 (PGE 2 ) on the phagocytosis of fluoroscein isothiocyanate (FITC)‐labelled Escherichia coli (O157) by human blood monocytes and U937 cells was studied by flow cytometry. Endotoxin increased the phagocytosis of labelled bacteria by both monocytes and U937 cells. IL‐1β and the polyunsaturated fatty acids; dihomo‐γ‐linolenic and arachidonic acids also increased the phagocytic activity of both monocytes and U937 cells. In contrast, PGE 2 suppressed phagocytosis in a concentration‐dependent manner. The cyclo‐oxygenase inhibitor, ketoprofen, further enhanced the increased phagocytic activity in the presence of endotoxin and interleukin‐1 (IL‐1) indicating suppression by endogenous prostaglandins. This was confirmed by the data which showed that lipopolysaccharide (LPS) and IL‐1 increased PGE 2 release and ketoprofen inhibited release. Endotoxin and fatty acids increased IL‐1β release also, whereas PGE 2 inhibited release. The data suggest that phagocytic activity may be linked to changes in IL‐1 levels. The data presented in this study also suggest that monocyte phagocytosis in the course of bacterial infection would be altered during pathophysiological events which result in elevation of extracellular fatty acids.