Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10145 (IL-8)
23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Germ-free ICR mice were mono- or dicontaminated with a multi-drug-resistant strain BIO-4R of Streptococcus faecalis (BIO-4R) and Escherichia coli 026 : K60 (E. coli) and administered aminobenzyl penicillin (ABPC). BIO-4R was established in the intestinal tract at a level of 10(8) viable cells per gram of stool on the fourth day following oral inoculation and the BIO-4R population was stably maintained thereafter. The drug resistance of BIO-4R remained unchanged in the intestinal tract of gnotobiotes throughout the experiment. Highly resistant cells of E. coli were isolated from the feces of some dicontaminated mice after ABPC administration. However, it seems that the high resistance of these E. coli is not due to the transfer of resistance of BIO-4R to E. coli. All animals given a large amount of BIO-4R (10(8) cells) per os survived throughout the study period of two weeks without symptoms.
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PMID:Studies on the establishment of multi-drug-resistant strain BIO-4R of Streptococcus faecalis in the intestinal tract of germ-free mice. Bacterial interaction and effect of antibiotics. 81 33

Cytokine mediators and leukocyte-endothelial cell adhesion molecules are critical and interdependent components of the acute inflammatory response in sepsis. We hypothesized that the administration of monoclonal antibodies to intercellular adhesion molecule-1 (CD54) or E- and L-selectin (CD62E/L) would decrease serum levels of the proinflammatory cytokines interleukin-1beta (IL-1), IL-6, and IL-8 and tumor necrosis factor receptor (TNFR-1) in baboons during sepsis. Adult male baboons received infusions of 1 x 10(9) colony forming units (CFU)/kg heat-killed Escherichia coli (E. coli) followed 12 h later by live E. coli (1 x 10(10) CFU/kg). At the time of live bacterial infusion, six septic animals were treated with a monoclonal antibody to CD54 and six with an antibody to CD62E and L (1 mg/kg). Eight untreated septic animals served as controls. Sequentially drawn serum samples were assayed for IL-1, IL-6, IL-8, and TNFR-1 using enzyme-linked immunoassay (ELISA). Data were compared using Mann-Whitney U tests and Chi-square analyses. Median survival was decreased in both treatment groups compared to controls (P < 0.05). Peak IL-1 level was higher than controls in septic animals treated with anti-CD54 but not anti-CD62E/L (P < 0.05, P = NS, respectively). Elevations in IL-6, IL-8, and TNFR-1 were increased and prolonged in both antibody treated groups compared to controls (P < 0.05). These results provide the first in vivo evidence that leukocyte-endothelial adhesion molecules CD54 and CD62E/L regulate cytokine production in sepsis.
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PMID:Proinflammatory cytokines increase in sepsis after anti-adhesion molecule therapy. 1080 17

Mutations in the Escherichia coli (E. coli) and Salmonella lpxM gene have been shown to result in strains which grow normally and which produce a non-myristoylated lipopolysaccharide (nmLPS) with strongly reduced endotoxicity. Using homologous recombination, we inactivated the lpxM gene in BL21 (DE3), a strain widely used for the production of recombinant proteins. This led to a derivative unaffected in its capacity to support the production of recombinant proteins. This new strain expresses non-myristoylated LPS that induces markedly less activation and maturation of monocyte-derived dendritic cells (DC), as assessed by nuclear translocation of nuclear factor kappa B (NF-kappaB), production of TNF-alpha and IL-8 or expression of CD86. Activation of the main signal transducing receptor for extracellular LPS, Toll like receptor (TLR) 4 in conjunction with the soluble accessory protein MD-2 was also markedly decreased. The modified BL21 strain represents a new application of lpxM inactivation for the expression of proteins to be tested on dendritic cells or other LPS sensitive cells/receptor complexes. It is likely to be useful for the identification of new proteins activating the innate immune response and to reducing the risk linked with low level of endotoxin contamination in therapeutic recombinant proteins.
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PMID:Expression of recombinant proteins in a lipid A mutant of Escherichia coli BL21 with a strongly reduced capacity to induce dendritic cell activation and maturation. 1250 24

Phagocytes are well-known effectors of the innate immune system to produce proinflammatory cytokines and chemokines such as tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1beta, and IL-8 during infections. Here, we show that infection of monocytes with wild-type Escherichia coli K1, which causes meningitis in neonates, suppresses the production of cytokines and chemokines (TNF-alpha, regulated on activation, normal T expressed and secreted, macrophage-inflammatory protein-1beta, IL-1beta, and IL-8). In contrast, infection of monocytes with a mutant E. coli, which lacks outer membrane protein A (OmpA- E. coli) resulted in robust production of cytokines and chemokines. Wild-type E. coli K1 (OmpA+ E. coli) prevented the phosphorylation and its degradation of inhibitor of kappaB, thereby blocking the translocation of nuclear factor (NF)-kappaB to the nucleus. OmpA+ E. coli-infected cells, subsequently subjected to lipopolysaccharide challenge, were crippled severely in their ability to activate NF-kappaB to induce cytokine/chemokine production. Selective inhibitors of the extracellular signal-regulated kinase (ERK) 1/2 pathway and p38 mitogen-activated protein kinase (MAPK), but not Jun N-terminal kinase, significantly reduced the activation of NF-kappaB and the production of cytokines and chemokines induced by OmpA- E. coli, indicating a role for these kinases in the NF-kappaB/cytokine pathway. It is interesting that the phosphorylation of ERK 1/2 and p38 MAPK was notably reduced in monocytes infected with OmpA+ E. coli when compared with monocytes infected with OmpA- E. coli, suggesting that the modulation of upstream events common for NF-kappaB and MAPKs by the bacterium is possible. The ability of OmpA+ E. coli K1 to inhibit the macrophage response temporarily may enable bacterial survival and growth within the host for the onset of meningitis by E. coli K1.
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PMID:Escherichia coli K1 inhibits proinflammatory cytokine induction in monocytes by preventing NF-kappaB activation. 1589 82

The expression of the proinflammatory cytokines interleukin-1beta (IL-1beta), IL-6, IL-8, and tumor necrosis factor-alpha (TNF-alpha) mRNAs was determined by reverse transcription-PCR (RT-PCR) analysis of biopsies from the mammary glands of sows. The biopsies were collected before and 24h after intramammary inoculation of 12 pregnant sows with Escherichia coli (E. coli). Four of the sows developed clinical signs of mastitis and these animals displayed significantly lower levels of IL-1beta mRNA before inoculation than those that remained clinically healthy. There was a significant increase in IL-1beta, IL-6, IL-8, and TNF-alpha mRNA expression in the inoculated mammary glands of sows that developed clinical signs of mastitis (affected group) 24h postinoculation. This was also true for IL-8 and TNF-alpha mRNA expression in the inoculated mammary glands of sows that did not develop clinical signs of mastitis (non-affected group). No significant differences were found in IL-1beta, IL-6, and TNF-alpha mRNA expression in the inoculated mammary glands between groups (affected versus non-affected) 24h postinoculation. Thus, a local production of proinflammatory cytokines in the mammary gland of sows was indicated by the induced expression of IL-1beta, IL-6, IL-8, and TNF-alpha mRNAs after intramammary inoculation with E. coli.
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PMID:Proinflammatory cytokine mRNA expression in mammary tissue of sows following intramammary inoculation with Escherichia coli. 1721 47

Phagocytic cells, comprised of neutrophils and monocytes/macrophages, play a key role in the innate immune response to infection. Our earlier study demonstrated that arabinoxylan rice bran (MGN-3/Biobran) activates murine peritoneal macrophage and macrophage cell lines. In this study, we investigated whether MGN-3 can upregulate the phagocytic activity of human phagocytes in peripheral blood to phagocytize Escherichia coli (E. coli), trigger the oxidative burst and produce cytokines. Phagocytic cells were pre-labeled with dichlorofluorescin diacetate dye and were incubated with phycoerythrin-labeled E. coli in the presence or absence of MGN-3. Phagocytosis and oxidative burst were assessed by flow cytometry. Results showed that treatment with MGN-3 enhanced the phagocytosis of E. coli by neutrophils and monocytes. This was associated with an increased oxidative burst. In addition, it caused a significant induction of cytokines (TNF-alpha, IL-6, IL-8 and IL-10); the effect was detected at 1 microg/ml and increased in a dose-dependent manner (P <or= 0.01). Notably, MGN-3 alone had no effect on the growth of 31 strains of bacteria suggesting that MGN-3 modulates phagocytic cellular function. These findings may have applications in the treatment of infections in the elderly and in immunocompromised patients.
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PMID:Modified arabinoxylan rice bran (MGN3/Biobran) enhances intracellular killing of microbes by human phagocytic cells in vitro. 1833 34

The aim of the present study was to determine postnatal ontogeny of proinflammatory cytokines IL-1beta, IL-8 and TNF-alpha production by in vitro stimulated porcine blood leukocytes. Four age categories of pigs were chosen. Cytokine production was determined using intracellular flow cytometry. It was found that IL-8 and TNF-alpha production by blood monocytes significantly increased during the postnatal period while production of IL-1beta remained unchanged. In blood neutrophils, the IL-8 production increased only during the postnatal period, while the levels of TNF-alpha and IL-1beta were undetectable during the whole postnatal period. Generally, the most intensive changes in cytokine production occurred before weaning. The production of low levels of cytokines by monocytes and neutrophils from young pigs was not caused by a delayed cytokine response because the cytokine production after 8-h stimulation was lower than that after 4-h stimulation in all age categories. The ontogenetical changes showed the same trends when two different stimulators (LPS, heat-inactivated E. coli) were used, suggesting that the ontogenetical changes are not caused by a simple defect in one signalling pathway, but it is probably a more complex process. No differences in cytokine production between the whole blood and the isolated cells supplemented with newborn or adult serum were found. Thus the ability of newborn monocytes and neutrophils to produce proinflammatory cytokines was not decreased due to the influence of composition of the microenvironment, where the cells were present. In conclusion, the ability of porcine blood leukocytes to produce cytokines develops during postnatal life.
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PMID:Age-dependent changes of proinflammatory cytokine production by porcine peripheral blood phagocytes. 1853 89

Toll-like receptors are essential pattern-recognition receptors of the innate immune system. They recognize a range of conserved molecules of invading microorganisms. The innate immune system is developed to protect the host, but can be deleterious if activated uncontrolled or inappropriate, such as in sepsis with Gram-negative bacteria. New approaches for treatment, like inhibition of innate immune responses, may be beneficial for the outcome of such conditions. Toll-like receptor 4 associated with CD14 and MD-2, is the lipopolysaccharide (LPS)-receptor and one of the candidates for such intervention. We investigated the newly described cyanobacterial LPS analogue CyP as a potential inhibitor of Escherichia coli (E. coli) LPS-induced inflammatory response in porcine whole blood. Pro-inflammatory cytokines and soluble terminal complement complex, sC5b-9, were used as read-outs. CyP, in contrast to E. coli LPS, did not induce cytokine production using doses up to 1mug/mL whole blood, indicating a lack of agonistic effect of CyP. In contrast, CyP was an efficient LPS antagonist, dose-dependently and completely inhibiting E. coli LPS-induced TNF-alpha, IL-1beta and IL-8 production. CyP was a modest activator of porcine complement compared to LPS from other Gram-negative bacteria. When CyP was pre-incubated in porcine whole blood before adding whole E. coli bacteria, a modest, variable and non-significant inhibition of cytokines were seen, reaching an average inhibition of 44% for IL-1beta. We have demonstrated for the first time that the cyanobacterial LPS analogue, CyP, is an efficient inhibitor of E. coli LPS-induced cytokines in whole blood and may be a candidate for therapeutic LPS-inhibition.
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PMID:Cyanobacterial LPS antagonist (CyP)-a novel and efficient inhibitor of Escherichia coli LPS-induced cytokine response in the pig. 1857 Dec 39

Urinary tract infection (UTI) is one of the most common sources of infection in children under 5. Rapid diagnosis is a need to avoid complications of UTI. The goal of the present study was to evaluate the use of urinary interleukin 8 (IL8) as a rapid laboratory method for diagnosis of UTI. A total of 116 children were included in the study. They were complaining of different diseases with pyuria. In addition twenty healthy children were included as control subjects. Urine samples were subjected to full chemical, cytological and bacteriological examinations. In addition, urinary IL8 was measured. Patients showed significantly elevated urine IL-8 levels (80-820 pg/ml) compared to control subjects (6-10 pg/ml) (p < 0.0001). There was significant correlation between interleukin 8 level and white blood cells counts in urine (p = 0.039). The mean +/- SD of urinary IL-8 was significantly increased 165.8 +/- 115.1 in urine with bacterial growth (Staphylococcus species and Escherichia coli) p < 0.001 than in urine without growth. Urine with Escherichia coli (E. coli) growth had significantly higher IL 8 level than growth with other types of organisms. The sensitivity, specificity, accuracy, positive predictive value and negative predictive value had higher level for IL8 compared to other parameters in urine examination i.e., nitrite, WBCs and RBCs (85.7%, 60%, 64%, 87%, 64% respectively). This study highlights that bacteriuria is associated with higher level of urinary interleukin 8 than pyuria without bacteriuria. Thus from this study we can conclude that IL8 can be used as rapid surrogate marker for rapid laboratory diagnosis of urosepsis.
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PMID:Interleukin 8 is a surrogate marker for rapid diagnosis of bacteriuria. 1882 Dec 16

The parasitic or commensal lifestyle of bacteria in different hosts depends on specific molecular interactions with the respective host species. In vitro models to study intestinal bacteria-host interactions in cattle are not available. Bovine primary colonocyte (PC) cultures were generated from colon crypt explants. Up to day 4 of culture, the vast majority of cells were of epithelial phenotype (i.e., expressed cytokeratin but not vimentin). PCs harboured mRNA specific for Toll-like receptors (TLR) 1, TLR3, TLR4 and TLR6 but not for TLR2, TLR5, TLR7, TLR8, TLR9 and TLR10. Six hours after inoculation of PC cultures with Escherichia coli (E. coli) prototype strains representing different pathovars (enterohaemorrhagic E. coli [EHEC], enteropathogenic E. coli [EPEC], enterotoxic E. coli [ETEC]), bacteria were found attached to the cells. EPEC adhesion was accompanied by intracellular actin accumulation. An attenuated laboratory strain (E. coli K12 C600) and a bovine commensal E. coli strain (P391) both did not adhere. Bacterial or LPS challenge of PC cultures resulted in specific increases in mRNA transcripts for IL-8, GRO-alpha, MCP-1, RANTES, and IL-10. The level of mRNA transcripts for TGF-beta stayed constant, while IL-12 mRNA was not detectable. Short-term cultures of PCs, maintaining epithelial cell properties, interacted with commensal and pathogenic bacteria in a strain-specific manner and have proven to be a useful in vitro model to study the interaction of bacteria with the bovine intestinal mucosa.
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PMID:Primary bovine colonic cells: a model to study strain-specific responses to Escherichia coli. 2047 Nov 9


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