Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Total serum iron, plasma lactoferrin and circulating leukocytes were measured in piglets during the early phase of severe gram-negative septicemia and endotoxemia in 3 experimental settings: intravenous (i.v.) infusion of lipopolysaccharide (LPS) (n = 8), i.v. infusion of live Escherichia coli (n = 7) and intraperitoneal (i.p.) infusion of E. coli (n = 6). Iron dropped significantly during the first 30 min of LPS infusion from a median of 32 microM to 13.4 microM. A similar decrease in serum iron was demonstrated in the 2 other groups with minimum values at 120 min after the start of E. coli infusion. Plasma levels of lactoferrin increased significantly 120 min after the start of LPS infusion (median 6 mg/l) when compared to preinfusion values (0.25 mg/l). After i.v. infusion of E. coli a significant rise of plasma lactoferrin was demonstrated already 30 min after bacterial infusion (to 2.1 mg/l) compared to preseptic values (0.8 mg/l). This increase was accompanied with a significant drop of circulating leukocytes (to 7.3 x 10(9)/l) compared to before the infusion (17 x 10(9)/l) in the pigs given E. coli i.v. After i.p. E. coli infusion no significant change of plasma lactoferrin was observed. The rapid fall of total serum iron seen during endotoxemia and E. coli septicemia may in part be explained by the release of lactoferrin from granulocytes and the clearance of iron-bound lactoferrin in the blood or peritoneal cavity.
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PMID:Early fall of circulating iron and rapid rise of lactoferrin in septicemia and endotoxemia: an early defence mechanism. 269 51

An experimental Escherichia coli septicaemia-peritonitis model was adapted to immunosuppressed mice. The mice were made neutropenic by a sublethal dose of cyclophosphamide, which resulted in a 100-fold increase in their susceptibility to intraperitoneal injection of E. coli O18:K1. A lethal infection could be prevented by passive immunisation with anti-K1 capsular or anti-O18 LPS antibodies but not with anti-J5 bacterial antibodies. The anti-K1 and anti-O18 antisera were able to increase the LD50 of the E. coli challenge by factors of 50 and 5, respectively. The role of non-specific, lipopolysaccharide (LPS)-mediated resistance to infection was also investigated in this model, in which only long-living phagocytic cells such as macrophages are believed to be functional. Pretreatment of mice with LPS was shown to prevent growth of the bacterial challenge in the peritoneal cavity and blood and to result in a five-fold increase in the LD50 of the challenge strain. These findings suggest an important role for macrophages as effector cells in defence against E. coli infection.
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PMID:Experimental Escherichia coli peritonitis in immunosuppressed mice: the role of specific and non-specific immunity. 327 82

Animal experiments were carried out to investigate whether a protective effect can be achieved in endotoxemia by intravenous (i.v.) application of a polyclonal immunoglobulin preparation (IVIG-IgG/A/M) enriched with 12% IgM and 12% IgA. Following administration of IVIG-IgG/A/M (500 mg/kg), endotoxemia was induced by intraperitoneal inoculation of a sublethal dose (5x10(8) CFU/kg) of Escherichia coli (E. coli) and subsequent i.v. administration of an antimicrobial agent (Imipenem). Plasma endotoxin activity, IL-6 activity, mean arterial pressure, and skeletal muscle oxygen pressure (tpO2) were measured at regular intervals over a total observation period of 7 h. Prophylactic administration of IVIG-IgG/A/M was found to significantly attenuate (P<0.01) the antibiotic-induced increase in endotoxin activity as compared to the albumin control group. Limited endotoxemia in the IgG/A/M group was associated with reduced levels of circulating IL-6 (P<0.01). Both lipopolysaccharide-induced hypotension and depression of tissue oxygenation were attenuated (P<0.01) by pre-treatment with IVIG-IgG/A/M. The experimental results suggest that in endotoxemia the polyclonal immunoglobulin preparation has a prophylactic protective effect on the acute phase responses and reduces the cardiodepressant effects of E. coli septicaemia.
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PMID:Protective capacity of a IgM/IgA-enriched polyclonal immunoglobulin-G preparation in endotoxemia. 1036 88