Premium
Heat‐Killed Salmonella typhi Induces the Release of Prostaglandins and Leukotrienes from Mouse Macrophages
Author(s) -
Pang Tikki,
Devi Shamala,
Puthucheary Savithri,
Pawlowski Nicholas
Publication year - 1991
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.1991.tb01556.x
Subject(s) - lipoxygenase , arachidonic acid , leukotriene , biology , eicosanoid , incubation , in vitro , arachidonate 5 lipoxygenase , oxygenase , salmonella typhi , hydroxyeicosatetraenoic acid , leukotriene c4 , leukotriene b4 , prostaglandin d2 , biochemistry , microbiology and biotechnology , prostaglandin , enzyme , inflammation , immunology , escherichia coli , asthma , gene
Mouse macrophages pre‐labeled with [ 3 H]arachidonic acid (20: 4) were shown to release metabolites generated by the lipoxygenase and cyclo‐oxygenase pathways following in vitro addition of heat‐killed Salmonella typhi. These metabolites were maximally released after 60–90 min of incubation and consisted of prostaglandins (85%), leukotriene C (6%), di‐HETEs, leukotrienes D and E (4%), mono‐HETEs (2%) and other metabolites (3%). Of the metabolites generated by the cyclo‐oxygenase pathway (prostaglandins), 6‐keto PGF1 α and PGE2 were generated at a ratio of 1.2 to 1. The significance and importance of these results are discussed.