Escherichia coli lipopolysaccharides diminish and enhance cell function of human polymorphonuclear leukocytes

Abstract

The effects of the lipopolysaccharide (LPS) of Escherichia coli J5 and 0111B4 on the function of human polymorphonuclear leukocytes (PMN) were tested. E. coli J5 is a UDP-galactose-4-epimerase-deficient mutant of E. coli 0111B4, and its LPS, therefore, contains mainly lipid A, as it lacks the polysaccharide side chains. PMN which had been incubated with J5 LPS showed decreased phagocytic, chemotactic, and metabolic activities as compared with control PMN. In contrast, incubation of PMN with 0111B4 LPS had no effect or even an enhancing effect on PMN function. When lipid A and the polysaccharide fraction were isolated from 0111B4 LPS, it was shown that lipid A had the same deleterious effect on PMN function as did J5 LPS and that the LPS fraction had no effect. When PMN were incubated with J5 LPS or lipid A, it could be shown that these structures were able to induce PMN to generate superoxide and chemiluminescence. 0111B4 LPS and the polysaccharide component were able to generate a metabolic burst by the PMN to a lesser extent. The induced defects in PMN function by J5 LPS could be prevented when polymyxin B or an oxygen-radical scavenger was present. We hypothesize that the lipid A portion of LPS is toxic for PMN due to the induction of toxic oxygen species by the PMN. These toxic oxygen species destroy the phagocytic, chemotactic, and metabolic activities of the PMN.

Chitin and chitosan stimulate canine polymorphonuclear cells to release leukotriene B4 and prostaglandin E2

“…32 Components of microorganisms such as LPS and zymosan induce PEF with a large number of inflammatory cells as a result of enhancing complement activities, synthesis of AAPs, and production of cytokines. 21,25,29,33 Our results showed that chitin and chitosan stimulated canine PMNs to release LTB 4 in vitro, and the SPEF contained enough LTB 4 to induce canine PMN migration. When NGIS and GIS were incubated for 3 h, however, the GIS contained more LTB 4 than the NGIS.…”

“…Additionally, the migratory activities induced by NGIS and GIS depended on the number of canine PMNs incubated with chitin and chitosan. PMNs play an important role in host defenses, not only by phagocytosis and bactericidal activity, 25 but also by producing chemical mediators and cytokines (such as LTB 4 and IL-8) when stimulated by invading microorganisms and other chemical mediators. 19,20 Many kinds of stimulants such as opsonized zymosan, lipopolysaccharide (LPS), and tumor necrosis factor cause neutrophils to release LTB 4 in vitro, 19,21,26,27 which enhances migration of PMNs.…”

The involvement of nitric oxide in the anti‐Candida albicans activity of rat neutrophils

“…LPS induces a variety of responses in phagocytic cells both in vitro and in vivo, 28,29 including priming of neutrophils to increase production of oxygen metabolites, which are thought to be involved in the neutrophil killing activity. 23 However, the fact that Candida does not induce superoxide anion production and the inability of LPS to prime rat elicited PMN to increase the oxygen radical generation may indicate that oxidative metabolites are not involved in the mechanism by which rat PMN kill C. albicans.…”

The chemoluminescence response of human polymorphonuclear leukocytes to Escherichia coli O and K antigens

“…The chemoluminescence response of PMN stimulated by the 01 antigen obtained from a pyelonephritopathogenic strain or by the 0 4 4 antigen obtained from an enteropathogenic strain was greater than the response to the other 0 antigens. Hernicks et al (29) reported that the chemolu-minescence response of PMN to 0 antigen stimulation originates from the lipid A component of the 0 antigen. However, the present finding of a varying chemoluminescence response to different 0 antigens indicates that the polysaccharide chain of the antigen may stimulate PMN to produce oxygen radicals.…”