Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been suggested that reducing the calcium content of peritoneal dialysis fluid (PDF) to 2.5 mEq/L decreases peritoneal macrophage (PMO) function and increases the incidence of peritonitis (especially Staphylococcus epidermidis peritonitis) in continuous ambulatory peritoneal dialysis patients. We studied the uptake and killing of S epidermidis and Escherichia coli by PMOs and peripheral blood leukocytes incubated in control buffer (Hank's balanced salt solution containing 0.1% gelatin [GHBSS]) and PDF containing varying concentrations of calcium (O to 3.5 mEq/L) and magnesium (O to 1.5 mEq/L) using ether diamine tetraacetic acid and ethylenediaminetetraacetic acid chelation, respectively. In addition, interleukin-1-beta-induced interleukin-6 production by human mesothelial cells was measured in the presence of concentrations of calcium increasing from 0 to 3.0 mmol/L. Fc receptor- mediated uptake of S epidermidis by PMO in the complete absence of Ca++ was comparable to that by PMO incubated in GHBSS with calcium. In contrast, the complement-dependent uptake of E coli was significantly lower in GHBSS devoid of Ca++ (46% +/- 5% v 24% +/- 3%; 0.05 < P < 0.02). No effect on intracellular killing of either microorganism by PMO was observed. The same held true for the phagocytic and killing capacity of polymorphonuclear granulocytes and monocytes obtained from healthy donors. Using Ca++ (2 to 3.5 mEq/L) and Mg++ (0.5 to 1.5 mEq/L) concentrations as applied in commercial PDFs, however, phagocytes performed as well as in control buffer. Interleukin-6 production by stimulated human mesothelial cells also required a small amount of Ca++ only, being normal above the 0.1 to 3 mmol/L Ca+ + range tested. Thus, complement- dependent uptake of bacteria by phagocytes is calcium dependent, whereas antibody-dependent uptake of S epidermidis is not. The concentrations of calcium in the current PDFs, however, will not compromise human mesothelial cells and leukocyte functions, and therefore should not impact the peritonitis rate.
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PMID:Low-calcium peritoneal dialysis fluid should not impact peritonitis rates in continuous ambulatory peritoneal dialysis. 860 11

Immune system alterations coexist with modifications in the reproductive axis. The bacterial endotoxin lipopolysaccharide (LPS) has inflammatory effects and stimulates cytokine release in the hypothalamus where LHRH neurons are located. LPS inhibition of LHRH release at hypothalamic level appears to be associated with modifications in the cerebral immune system. Central and peripheral LPS administration induces the expression and release of several cytokines in the central nervous system. Hence the present study was designed to investigate a possible function of the interleukin-6 (IL-6) stimulated by LPS in the regulation of LHRH secretion. Male rats were decapitated, and the preoptic mediobasal hypothalamic area (PO/MBH) was dissected and superfused with Earle's balanced salt solution. Superfusate fractions were collected at 15-min intervals after a 60-min stabilization superfusion period. LPS (100 ng/ml) and IL-6 receptor antagonist (IL-6ra) were then added to the superfusion medium over 1 h in two different experimental designs: (1) LPS only and (2) LPS followed by IL-6ra, performed in different experiments. This was followed by a washout period. The PO/MBH fragments were then subjected to a 56 mM K+ stimulus. Control PO/MBH fragments were continuously superfused with Earle's solution. As expected, LHRH release was significantly reduced (p < 0.05) during and following exposure to LPS. At the same time, IL-6 concentrations significantly increased in the superfusion medium compared with the control group. IL-6ra significantly (p < 0.01) potentiated the inhibitory effect of LPS on LHRH secretion. On the bases of previous papers indicating a stimulatory effect of IL-6 on LHRH release it could be considered that the potentiation of IL-6ra of the inhibitory effect of LPS on LHRH could be the consequence of the lack of the stimulatory effect of IL-6 on LHRH produced by the receptor antagonist. IL-6ra also increased IL-6 levels measured in medium probably due to a decrease in the metabolization induced by the blockage of the receptors and the consequent accumulation of IL-6 in the media. These results could indicate that IL-6 partly attenuates the inhibitory effect of LPS on LHRH release. These observations indicate that there is an increase in IL-6 release that becomes significant at the same time when LHRH release is decreased. Also, depolarizing concentrations of K+ (56 mM) did not increase IL-6 release, while LHRH release from the hypothalamic fragments was significantly increased. These data suggest that the inhibitory effect of LPS on LHRH release may be explained by the stimulation of other cytokines than IL-6, meanwhile the augmented levels of IL-6 probably released via a nonneuronal source was shown to be higher when LHRH was decreased. This could confirm the stimulatory role of IL-6 on LHRH release.
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PMID:Hypothalamic relationships between interleukin-6 and LHRH release affected by bacterial endotoxin in adult male rats. Involvement of the inhibitory amino acid system 958 21

Immune system alterations coexist with modifications in the reproductive axis. The bacterial endotoxin lipopolysaccharide (LPS) has inflammatory effects and stimulates cytokine release in the hypothalamus where LHRH neurons are located. LPS inhibition of LHRH release at hypothalamic level appears to be associated with modifications in the cerebral immune system. Central and peripheral LPS administration induces the expression and release of several cytokines in the central nervous system. Hence the present study was designed to investigate a possible function of the interleukin-6 (IL-6) stimulated by LPS in the regulation of LHRH secretion. Male rats were decapitated, and the preoptic mediobasal hypothalamic area (PO/MBH) was dissected and superfused with Earle's balanced salt solution. Superfusate fractions were collected at 15-min intervals after a 60-min stabilization superfusion period. LPS (100 ng/ml) and IL-6 receptor antagonist (IL-6ra) were then added to the superfusion medium over 1 h in two different experimental designs: (1) LPS only and (2) LPS followed by IL-6ra, performed in different experiments. This was followed by a washout period. The PO/MBH fragments were then subjected to a 56 mM K+ stimulus. Control PO/MBH fragments were continuously superfused with Earle's solution. As expected, LHRH release was significantly reduced (p < 0.05) during and following exposure to LPS. At the same time, IL-6 concentrations significantly increased in the superfusion medium compared with the control group. IL-6ra significantly (p < 0.01) potentiated the inhibitory effect of LPS on LHRH secretion. On the bases of previous papers indicating a stimulatory effect of IL-6 on LHRH release it could be considered that the potentiation of IL-6ra of the inhibitory effect of LPS on LHRH could be the consequence of the lack of the stimulatory effect of IL-6 on LHRH produced by the receptor antagonist. IL-6ra also increased IL-6 levels measured in medium probably due to a decrease in the metabolization induced by the blockage of the receptors and the consequent accumulation of IL-6 in the media. These results could indicate that IL-6 partly attenuates the inhibitory effect of LPS on LHRH release. These observations indicate that there is an increase in IL-6 release that becomes significant at the same time when LHRH release is decreased. Also, depolarizing concentrations of K+ (56 mM) did not increase IL-6 release, while LHRH release from the hypothalamic fragments was significantly increased. These data suggest that the inhibitory effect of LPS on LHRH release may be explained by the stimulation of other cytokines than IL-6, meanwhile the augmented levels of IL-6 probably released via a nonneuronal source was shown to be higher when LHRH was decreased. This could confirm the stimulatory role of IL-6 on LHRH release.
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PMID:Hypothalamic relationships between interleukin-6 and LHRH release affected by bacterial endotoxin in adult male rats. Involvement of the inhibitory amino acid system. 964 93

Administration of pyruvate, an effective scavenger of reactive oxygen species, has been shown to be salutary in numerous models of redox-mediated tissue or organ injury. Pyruvate, however, is unstable in solution and, hence, is not attractive for development as a therapeutic agent. Herein, ethyl pyruvate, which is thought to be more stable than the parent compound, was formulated in a calcium-containing balanced salt solution [Ringer ethyl pyruvate solution (REPS)] and evaluated in a murine model of hemorrhagic shock and resuscitation (HS/R). Resuscitation with REPS instead of Ringer lactate solution (RLS) significantly improved survival at 24 h and abrogated bacterial translocation to mesenteric lymph nodes and the development of increased ileal mucosal permeability to FITC-labeled dextran (4,000 Da) at 4 h. Mice treated with REPS instead of RLS also had lower circulating levels of alanine aminotransferase at 4 h. Treatment with REPS instead of RLS decreased activation of nuclear factor-kappaB in liver and colonic mucosa after HS/R and also decreased the expression of inducible nitric oxide synthase, tumor necrosis factor, cyclooxygenase-2, and interleukin-6 mRNA in liver, ileal mucosa, and/or colonic mucosa. These data support the view that resuscitation with REPS modulates the inflammatory response and decreases hepatocellular and gut mucosal injury in mice subjected to HS/R.
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PMID:Ethyl pyruvate modulates inflammatory gene expression in mice subjected to hemorrhagic shock. 1206 9