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)

Colony-stimulating factors are a family of glycoproteins instrumental in regulation of hematopoiesis and inflammation. Clinical effects of various colony-stimulating factors have been reported in murine and human hosts. This review summarizes findings from some clinical trial evaluations of macrophage colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, granulocyte colony-stimulating factor, interleukin-1, interleukin-3, interleukin-4, interleukin-5, interleukin-6, and interleukin-7 administration to other species. These factors stimulate clonal expansion of progenitor cells in the bone marrow, induce differentiation of various cell lineages to a mature phenotype, and, in some cases, enhance the effector activities of immune cells. Each colony-stimulating factor has distinct lineages of bone marrow cells upon which they act, although there is some overlap in lineage activity and synergy between colony-stimulating factors. The close relationship in biological activity among different colony-stimulating factors is also reflected at the genomic level at which genes for some hematopoietic growth factors have been mapped to a region of human chromosome 5. Recently, colony-stimulating factor administration to cattle and its potential application to disease control in bovine preventive medicine programs has been investigated. Data from recent hematological, immunological, and intramammary bacterial (Staphylococcus aureus and Klebsiella pneumoniae) challenge studies in dairy cows are reviewed. These studies, with limited numbers of cows, found that rate of new infections, as well as duration and severity of infection, were reduced by pretreatment of cows with granulocyte-colony stimulating factor. The dose-dependent hematological and immunomodulatory effects of granulocyte colony-stimulating factor administration may explain reduced severity and incidence of mastitis in dairy cows given granulocyte colony-stimulating factor.
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PMID:Immunobiology of hematopoietic colony-stimulating factors: potential application to disease prevention in the bovine. 172 1

The present study was designed to investigate the effect of membrane proteoglycans (MPG) from Klebsiella pneumoniae on IL-6 production by human peripheral blood monocytes. Exposure in vitro to MPG induced release of IL-6 activity from human monocytes, as assessed by the 7TD1 hybridoma assay. MPG-induced hybridoma growth factor activity was blocked by anti-IL-6 antibodies. MPG induced expression in human monocytes of IL-6 mRNA transcripts as assessed by Northern blot analysis. Induction of IL-6 in mononuclear phagocytes may play a role in the immunomodulatory activity of MPG.
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PMID:Interleukin-6 gene expression and production induced in human monocytes by membrane proteoglycans from Klebsiella pneumoniae. 220 91

In this paper, the effects of recombinant human interleukin-1 (IL-1) on non-specific resistance to infection are reviewed. In experiments in neutropenic mice, a single injection of a low dose of IL-1 (8-800 ng) appears to protect against death from lethal Pseudomonas aeruginosa and Candida albicans infections. In non-neutropenic mice protection can also be obtained with such dosages of IL-1 in infection caused by Klebsiella pneumoniae or Listeria monocytogenes. Low dosages of IL-1 are also able to prevent lethal cerebral malaria in mice. No effect has been found in murine cytomegalovirus infection. With the exception of C. albicans infection and malaria, protection is only obtained if IL-1 is given before the infection. The mechanism of protection has not been elucidated; in the Pseudomonas and Klebsiella infection, it could be demonstrated that survival was not due to a direct antibacterial effect of IL-1, not due to the action of granulocytes or increased hematopoietic recovery and not due to activation of macrophages and increased bactericidal mechanisms. In the experimental Listeria infection however, animals treated with IL-1 had lower bacterial counts in their organs. Since the cytokines interleukin-6 (IL-6) and tumor necrosis factor (TNF) are much less potent than IL-1 in these protection experiments, it is very unlikely that they are endogenous mediators of the protection induced by IL-1. The effect is not mediated via the cyclooxygenase pathway, since premedication with ibuprofen does not influence the protective effect of IL-1. Taking these data together, it is felt that IL-1 holds promise as a therapeutic agent in humans.
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PMID:Options for the treatment of serious infections with interleukin-1. 270 46

Infections by gram-negative bacteria are one of the major causes of death in newborns. Bacterial clearance is deficient in septic neonates, which seems to increase their susceptibility to infections. In this study, we observed a significant improvement in clearance of Klebsiella pneumoniae in newborn wistar rats inoculated by intraperitoneal via with 800 mg k soybean phosphatidylcholine (PC), compared to the control group injected with PBS (p 0.05). The overall survival rate was improved (p 0.05) and the white blood cell counts showed a greater leukocytosis and neutrophilia during the peak of bacteremia in the PC treated animals. Circulating levels of interleukin-6 were greater in the PC group, which developed an intense splenic hematopoiesis of the granulocyte (p 0.05) and megakariocyte series (p 0.01). No significant changes were observed in bone marrow granulocyte deposits in both study groups. The improvement in survival rate, the changes in leukocyte counts and the splenic hematopoiesis may be associated with the increased production of IL-6. These results suggest that IL-6 plays a role in the protection mechanism induced by PC in this experimental model of newborn septicemia. PC seems to be an immunomodulator of the acute response to gram-negative bacterial infection.
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PMID:[Phosphatidylcholine induces an increase in the production of interleukin-6 and improves survival of rats with neonatal sepsis caused by Klebsiella pneumoniae]. 749 35

Concordance between gram-negative enteric and other toxin-producing bacteria in blood and stool culture, endotoxin (lipopolysaccharide), and interleukin-6 (IL-6) was measured in 60 preterm infants (600-1600 g) as a clinical index in neonatal necrotizing enterocolitis (NEC). E. coli, Klebsiella, Enterobacter, and Clostridium spp., identified by routine bacteriology, were each strongly associated with elevated concentrations of endotoxin (P < 0.01) in stool filtrates, with Clostridium spp. most strongly associated with NEC disease. Stool filtrate endotoxin (EU/g) measured by a Limulus amebocyte lysate assay was age dependent. Samples from stage I NEC (61%) and infants with advanced disease (67%) had notably elevated levels of stool endotoxin (> 10 ln EU/g) compared to NEC-negative (47%) samples tested. Plasma and stool IL-6 generally tested at the low, nonmeasurable limit of the ELISA for NEC-negative (88%) and stage I NEC (93%), although a small proportion of samples (25%) from infants with stage II or III NEC had elevated stool concentrations of IL-6. We conclude that identification of toxin-producing organisms and endotoxin elevations in stool filtrates are more useful than circulating levels of endotoxin in plasma in predicting mucosally limited disease in the gastrointestinal tract. The prognostic value of monitoring stool endotoxin in infants with overgrowth of gram-negative bacteria has implications for therapeutic strategies in patients with early and advanced stages of disease. Monitoring inflammatory cytokines (IL-6) in relation to endotoxin values in stool appears of limited clinical value in controlling this devastating disease in preterm neonates.
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PMID:Concordance of bacterial cultures with endotoxin and interleukin-6 in necrotizing enterocolitis. 905 20

The role of bacterial capsule in inflammatory responses in experimentally induced pneumonia caused by Klebsiella pneumoniae was evaluated by comparing the host immunological responses in mice infected with capsulate strain DT-S and non-capsulate mutant strain DT-X. Anaesthetised ICR mice were infected intranasally with inocula of strain DT-S or DT-X. Mice infected with strain DT-X survived significantly longer than those inoculated with strain DT-S. Viable bacterial counts in lungs and blood increased rapidly in mice infected with strain DT-S, in contrast to the gradual decrease in their density in lungs and intermittent bacteraemia in mice infected with strain DT-X. The number of broncho-alveolar lavage (BAL) cells in mice infected with strain DT-X at 24 h after inoculation was significantly higher than in those infected with strain DT-S. In the early stages of infection, the levels of tumour necrosis factor-a and interleukin-6 in BAL fluid of mice infected with strain DT-X were significantly higher than those of mice infected with strain DT-S. In contrast, in the late stage of infection, the levels of these cytokines in serum of mice infected with strain DT-S were significantly higher than in mice infected with strain DT-X. These results suggest that K. pneumoniae capsule may suppress the host immunological responses,thus allowing the bacteria to grow, causing pneumonia, septicaemia and death.
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PMID:Role of bacterial capsule in local and systemic inflammatory responses of mice during pulmonary infection with Klebsiella pneumoniae. 1107 54

OBJECTIVE: To investigate the production of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) induced by live Gram-negative and Gram-positive bacteria in whole blood in vitro. METHODS: In all, 49 different isolates were studied. Each of the 49 different isolates was incubated for 4 h with whole blood at a ratio of one monocyte per 1--5 bacteria. Plasma was then separated and frozen, and the concentrations of TNF-alpha and IL-6 were measured by enzyme immunoassays. RESULTS: There was a positive correlation between TNF-alpha and IL-6 values, r=0.9. Gram-negative bacteria induced higher levels of both TNF-alpha and IL-6 than Gram-positive bacteria. Group G streptococci (GGS) induced higher levels of TNF-alpha than Streptococcus pneumoniae, Staphylococcus aureus, Staphylococcus epidermidis and group A streptococci (GAS). Klebsiella pneumoniae induced higher levels of TNF-alpha than Haemophilus influenzae, Escherichia coli and Neisseria meningitidis. GGS induced higher levels of IL-6 than Staphylococcus epidermidis, Staphylococcus aureus and GAS. When the relative amounts of cytokine induced by the strains were compared to serum concentrations measured on admission in patients with bacteremia caused by the same bacterial isolates there was no significant correlation. CONCLUSION: Species- and strain-related differences in cytokine-inducing properties were found which may have significance in clinical infections.
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PMID:Production of tumor necrosis factor-alpha and interleukin-6 in whole blood stimulated by live Gram-negative and Gram-positive bacteria. 1186 6

Mammalian cathelicidins are a class of innate antimicrobial peptides isolated from leukocytes and epithelial cells that aid host defense against bacterial infections. Synthetic analogs of cathelicidins offer the promise of potent broad-spectrum antimicrobial efficacy. We developed a combined lung infection and ex vivo whole-blood assay model to characterize the toxicity and efficacy of synthetic cathelicidin-derived peptides. Male C57BL/6 mice were administered saline or Klebsiella pneumoniae by intratracheal instillation. Five hours later, the Klebsiella-infected mice were instilled with saline, tobramycin (1 mg/kg of body weight or 10 mg/kg), novispirin G10 (0.4 mg/kg), or a combination of tobramycin (1 mg/kg) and G10 (0.4 mg/kg). At 24 h, bronchoalveolar lavage fluid (BAL) was collected for analysis of culturable bacteria and for markers of inflammation and lung toxicity. Blood samples were analyzed for circulating cytokines. Recovery of Klebsiella from the lung, recruitment of neutrophils, and production of interleukin-6 (IL-6) in BAL samples were highly correlated (r=0.68 and 0.84, respectively; P<0.01). Animals treated with G10 or G10 plus tobramycin had increased hemoglobin (P<0.001) and protein (P<0.001) levels compared to those for Klebsiella-infected or tobramycin-alone-treated animals. The levels of circulating IL-6 in mice infected with Klebsiella were 1000- to 10,000-fold higher than in the noninfected controls. The highest levels of IL-6 were measured in mice given G10 alone or in combination with tobramycin. These studies demonstrated that G10 was relatively nontoxic in saline-treated mice but was highly toxic in mice infected with Klebsiella. This finding establishes the importance of investigating candidate antimicrobial agents in an in vivo infection model.
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PMID:Novispirin G10-induced lung toxicity in a Klebsiella pneumoniae infection model. 1463

N-acetylcysteine (NAC) is an antioxidant and cytoprotective agent with scavenging action against reactive oxygen species and inhibitory effects on pro-inflammatory cytokines. In a previous study, we found that pretreatment with NAC attenuated organ dysfunction and damage, reduced the production of free radicals, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) following endotoxemia elicited by administration of lipopolysaccharide (LPS). In the present study, we tested the effects of post-treatment with NAC on the sepsis-induced change. Post-treatment imitates clinical therapeutic regimen with administration of drug after endotoxemia. Endotoxin shock was induced by intravenous injection of Klebsiella pneumoniae LPS (10 mg/kg) in conscious rats. Mean arterial pressure (MAP) and heart rate (HR) were continuously monitored for 48 h after LPS administration. NAC was given 20 min after LPS. Measurements of biochemical substances were taken to reflect organ functions. Biochemical factors included blood urea nitrogen (BUN), creatinine (Cre), lactate dehydrogenase (LDH), creatine phosphokinase (CPK), aspartate transferase (GOT), alanine transferase (GPT), TNF-alpha, interleukin-6 (IL-6), and interleukin-10 (IL-10). LPS significantly increased blood BUN, Cre, LDH, CPK, GOT, GPT, TNF-alpha, IL-6, IL-10 levels and HR, and decreased MAP. Post-treatment with NAC diminished the decrease in MAP, increased the HR, and decreased the markers of organ injury (BUN, Cre, LDH, CPK, GOT, GPT) and inflammatory biomarkers (TNF-alpha, IL-6, IL-10) after LPS. We conclude that post-treatment with NAC suppresses the release of plasma TNF-alpha, IL-6, and IL-10 in endotoxin shock, and decreases the markers of organ injury. These beneficial effects protect against LPS-induced kidney, heart and liver damage in conscious rats. The beneficial effects may suggest a potential chemopreventive effect of this compound after sepsis.
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PMID:Post-treatment with N-acetylcysteine ameliorates endotoxin shock-induced organ damage in conscious rats. 1686 Mar 47

Yersinia pestis is the causative agent of plague, a disease that can manifest as either bubonic or pneumonic plague. An interesting feature of plague is that it is a rapidly progressive disease, suggesting that Y. pestis either evades and/or suppresses the innate immune response to infection. Therefore, the early host response during the course of primary pneumonic plague was investigated in two mouse strains, the outbred strain CD1 and the inbred strain C57BL/6. A comparative analysis of the course of disease in these two strains of mice indicated that they are susceptible to intranasal Y. pestis CO92 infection and have similar 50% lethal doses and kinetics of infection with respect to colonization of the lung, liver, and spleen. Significantly, in both strains of mice, robust neutrophil recruitment to the lungs was not observed until 48 h after infection, suggesting that there was a delay in inflammatory cell recruitment to the site of infection. In addition, proinflammatory cytokines (interleukin-6 [IL-6], tumor necrosis factor alpha, gamma interferon, IL-12p70, monocyte chemoattractant protein 1) and chemokines (KC, MIP-2) in the bronchoalveolar lavage fluids were not readily detected until 48 h after infection, which coincided with the increase in polymorphonuclear leukocyte (PMN) recruitment to the lungs. In comparison, CD1 mice with gram-negative pneumonia caused by Klebsiella pneumoniae exhibited strong inflammatory responses early in infection, with PMNs comprising the majority of the cells in the bronchoalveolar lavage fluid 24 h postinfection, indicating that PMN recruitment to the lungs could occur earlier in this infection than in Y. pestis infection. Together, our results indicate that there is a delay in the recruitment of neutrophils to the lungs in the mouse model of primary plague pneumonia that correlates with delayed expression of proinflammatory cytokines and chemokines in both outbred and inbred mice.
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PMID:Delayed inflammatory response to primary pneumonic plague occurs in both outbred and inbred mice. 1710 42


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