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Titolo:
PROSTAGLANDIN AND FATTY-ACID MODULATION OF ESCHERICHIA-COLI O157 PHAGOCYTOSIS BY HUMAN MONOCYTIC CELLS
Autore:
DAVIDSON J; KERR A; GUY K; ROTONDO D;
Indirizzi:
UNIV STRATHCLYDE,DEPT IMMUNOL GLASGOW G4 0NR LANARK SCOTLAND
Titolo Testata:
Immunology
fascicolo: 2, volume: 94, anno: 1998,
pagine: 228 - 234
SICI:
0019-2805(1998)94:2<228:PAFMOE>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTERLEUKIN-1 INDUCES INTERLEUKIN-1; MONONUCLEAR-CELLS; LEUKOCYTES; BACTERIAL; ENDOTOXIN; RELEASE; GAMMA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
16
Recensione:
Indirizzi per estratti:
Citazione:
J. Davidson et al., "PROSTAGLANDIN AND FATTY-ACID MODULATION OF ESCHERICHIA-COLI O157 PHAGOCYTOSIS BY HUMAN MONOCYTIC CELLS", Immunology, 94(2), 1998, pp. 228-234

Abstract

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-1 beta (IL-1 beta), fatty acids and prostaglandin E-2 (PGE(2)) on the phagocytosis of fluoroscein isothiocyanate (FITC)-labelled Escherichia coil (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-1 beta and the polyunsaturated fatty acids; dihomo-gamma-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-1 beta 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.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/10/20 alle ore 08:52:55