UNIPROT:P10145 - FACTA Search

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Query: UNIPROT:P10145 (IL-8)
23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty consecutive patients scheduled for elective colorectal surgery were prospectively randomized to receive either filgrastim [the recombinant human form of granulocyte colony-stimulating factor (r-metHu-G-CSF)] or placebo blindly. The levels of interleukin (IL-)1beta, tumour necrosis factor-alpha (TNF-alpha), IL-6, IL-8, transforming growth factor-beta (TGF-beta), and IL-10 were determined 5 and 24 h postoperatively from peripheral blood, peritoneal fluid, and wound fluid. The concentrations of all the measured cytokines were enormously higher locally at the operative site than in the systemic circulation. The only difference between the two medication groups was the lower concentration of IL-8 in peripheral blood in the filgrastim-treated patients. The present study shows abundant release of pro- and anti-inflammatory cytokines into the wound and the peritoneal cavity after abdominal surgery. The systemic response to surgery seems to be a secondary and minor reflection of local events. Filgrastim did not have any effect on the studied local cytokine levels at the operative site.
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PMID:Maximal local and minimal systemic cytokine response to colorectal surgery: the influence of perioperative filgrastim. 1139 98

Nontypeable Hemophilus influenzae (NTHi) is an important human pathogen in both children and adults. In children, it causes otitis media, the most common childhood infection and the leading cause of conductive hearing loss in the United States. In adults, it causes lower respiratory tract infections in the setting of chronic obstructive pulmonary disease, the fourth leading cause of death in the United States. The molecular mechanisms underlying the pathogenesis of NTHi-induced infections remain undefined, but they may involve activation of NF-kappa B, a transcriptional activator of multiple host defense genes involved in immune and inflammatory responses. Here, we show that NTHi strongly activates NF-kappa B in human epithelial cells via two distinct signaling pathways, NF-kappa B translocation-dependent and -independent pathways. The NF-kappa B translocation-dependent pathway involves activation of NF-kappa B inducing kinase (NIK)--IKK alpha/beta complex leading to I kappa B alpha phosphorylation and degradation, whereas the NF-kappa B translocation-independent pathway involves activation of MKK3/6--p38 mitogen-activated protein (MAP) kinase pathway. Bifurcation of NTHi-induced NIK-IKK alpha/beta-I kappa B alpha and MKK3/6--p38 MAP kinase pathways may occur at transforming growth factor-beta activated kinase 1 (TAK1). Furthermore, we show that toll-like receptor 2 (TLR2) is required for NTHi-induced NF-kappa B activation. In addition, several key inflammatory mediators including IL-1 beta, IL-8, and tumor necrosis factor-alpha are up-regulated by NTHi. Finally, P6, a 16-kDa lipoprotein highly conserved in the outer membrane of all NTHi and H. influenzae type b strains, appears to also activate NF-kappa B via similar signaling pathways. Taken together, our results demonstrate that NTHi activates NF-kappa B via TLR2-TAK1-dependent NIK--IKK alpha/beta-I kappa B alpha and MKK3/6--p38 MAP kinase signaling pathways. These studies may bring new insights into molecular pathogenesis of NTHi-induced infections and open up new therapeutic targets for these diseases.
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PMID:Activation of NF-kappa B by nontypeable Hemophilus influenzae is mediated by toll-like receptor 2-TAK1-dependent NIK-IKK alpha /beta-I kappa B alpha and MKK3/6-p38 MAP kinase signaling pathways in epithelial cells. 1143

During normal pregnancy, a predominance of Th2 type cytokines prevails and is considered to protect the fetus. Animal experiments suggest that an increase of Th1 type cytokines may instead have deleterious effects. We have studied with the reverse transcription PCR technique mRNA for IL-1alpha, IL-1beta, IL-6, IL-8, IL-10, transforming growth factor-beta, tumor necrosis factor-alpha, and interferon-gamma in placentas from full-term appropriately grown newborns, newborns with intrauterine growth retardation (IUGR) and newborns who were only small for gestational age. The mRNA for IL-10 was significantly reduced in the IUGR placentas (p < 0.05), whereas the mRNA for IL-8 was significantly higher (p < 0.05) for the IUGR cases compared with the full-term neonates. It might be that reduced IL-10 in the placenta is involved in the pathogenesis of IUGR.
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PMID:Aberrations in placental cytokine mRNA related to intrauterine growth retardation. 1180 15

In murine systems, the B subunit of Escherichia coli heat-labile enterotoxin (EtxB) is a potent immunomodulator capable of suppressing Th1-mediated autoimmune diseases. This results from its ability to bind cell surface receptors, principally GM1-ganglioside, and as a consequence down-regulate the pathological T helper type 1 (Th1) response. The capacity of EtxB to alter human T-cell responses has not been investigated. Here we show that EtxB, but not the receptor non-binding mutant EtxB (G33D), triggers the release of interleukin (IL)-10, IL-6 and tumour necrosis factor-alpha (TNF-alpha) by human monocytes. The production of IL-8, transforming growth factor-beta (TGF-beta) or IL-12 was not enhanced by EtxB. Indeed, EtxB was shown to inhibit IL-12 secretion in monocytes stimulated with interferon-gamma (IFN-gamma) and lipopolysaccharide (LPS) by an IL-10-independent mechanism. When EtxB-treated monocytes were used as antigen presenting cells in an allogeneic mixed lymphocyte reaction (MLR), IL-10 and IFN-gamma production were increased in comparison to levels seen in cultures stimulated with untreated monocytes; proliferation was unaltered. This modulation of the T-cell response was not only evident in the primary MLR triggered by EtxB-treated monocytes, but also upon restimulation of the responding T cells with fresh untreated monocytes; indicating that presentation by EtxB-treated monocytes leads to altered T-cell differentiation. Sorting experiments showed that IL-10 secreting T cells from the MLR cultures were strong suppressors of T-cell proliferation following their addition into a fresh primary MLR.
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PMID:Modulation of human monocytes by Escherichia coli heat-labile enterotoxin B-subunit; altered cytokine production and its functional consequences. 1210 Jul 19

Enriched populations of human microglial cells were isolated from mixed cell cultures prepared from embryonic human telencephalon tissues. Human microglial cells exhibited cell type-specific antigens for macrophage-microglia lineage cells including CD11b (Mac-1), CD68, B7-2 (CD86), HLA-ABC, HLA-DR and ricinus communis aggulutinin lectin-1 (RCA-1), and actively phagocytosed latex beads. Gene expression and protein production of cytokines, chemokines and cytokine/chemokine receptors were investigated in the purified populations of human microglia. Normal unstimulated human microglia expressed constitutively mRNA transcripts for interleukin- 1beta (IL-1beta) -6, -8, -10, -12, -15, tumor necrosis factor-alpha (TNF-alpha), macrophage inflammatory protein-1alpha (MIP-1alpha), MIP-1beta, and monocyte chemoattractant protein-1 (MCP-1), while treatment with lipopolysaccharide (LPS) or amyloid beta peptides (Abeta) led to increased expression of mRNA levels of IL-8, IL-10, IL-12, TNF-alpha, MIP-1alpha, MIP-1beta, and MCP-1. Human microglia, in addition, expressed mRNA transcripts for IL-1RI, IL-1RII, IL-5R, IL-6R, IL-8R, IL-9R, IL-10R, IL-12R, IL-13R, and IL-15R. Enzyme-linked immunosorbent assays (ELISA) showed increased protein levels in culture media of IL-1beta, IL-8, TNF-alpha, and MIP-1alpha in human microglia following treatment with LPS or Abeta. Increased TNF-alpha release from human microglia following LPS treatment was completely inhibited with IL-10 pretreatment, but not with IL-6, IL-9, IL-12, IL-13, or transforming growth factor-beta (TGF-beta). Present results should help in understanding the basic microglial biology, but also the pathophysiology of activated microglia in neurological diseases such as Alzheimer disease, Parkinson disease, Huntington disease, amyotrophic lateral sclerosis, stroke, and neurotrauma.
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PMID:Cytokines, chemokines, and cytokine receptors in human microglia. 1211 20

Chronic obstructive pulmonary disease (COPD) is characterized by chronic obstruction of expiratory flow affecting peripheral airways, associated with chronic bronchitis (mucus hypersecretion with goblet cell and submucosal gland hyperplasia) and emphysema (destruction of airway parenchyma), together with fibrosis and tissue damage, and inflammation of the small airways. Cytokines are extracellular signalling proteins. Increased levels of interleukin (IL)-6, IL-1beta, tumour necrosis factor-alpha (TNF-alpha) and IL-8 have been measured in sputum, with further increases during exacerbations, and the bronchiolar epithelium over-expresses monocyte chemotactic protein (MCP)-1 and IL-8. IL-8 can account for some chemotactic activity of sputum, and sputum IL-8 levels correlate with airway bacterial load and blood myeloperoxidase levels. The expression of chemokines such as regulated on activation, normal T-cell expressed and secreted (RANTES) may underlie the airway eosinophilia observed in some COPD patients. Cytokines may be involved in tissue remodelling. TNF-alpha and IL-1beta stimulate macrophages to produced matrix metalloproteinase-9 (MMP-9), and bronchial epithelial cells to produce extracellular matrix glycoproteins such as tenascin. Increased expression of transforming growth factor-beta (TGFbeta) and of epidermal growth factor (EGF) occurs in the epithelium and submucosal cells of patients with chronic bronchitis. TGFbeta and EGF activate proliferation of fibroblasts, while activation of the EGF receptor leads to mucin gene expression. The cytokine profile seen in chronic obstructive pulmonary disease is different from that observed in asthma. The role of these cytokines needs to be defined and there is a potential for anticytokine therapy in chronic obstructive pulmonary disease.
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PMID:Cytokines in chronic obstructive pulmonary disease. 1239 35

Canine cells of different histogenesis were infected with the Onderstepoort strain of distemper virus (CDV) to study the effect of viral infection on cytokine production. Included were primary brain cells, dermal fibroblasts, and two cell lines, DH 82 cells (macrophage-like) and epithelial Madin-Darby canine kidney (MDCK) cells. All cultures produced infective virus. MDCK cells had the lowest percentage of CDV-antigen positive cells, and infection did not cause a significant increase of cell death. After infection, mRNA steady state levels of interleukin (IL)-1, IL-6, IL-8, IL-12, tumor necrosis factor-alpha (TNF), and transforming growth factor-beta (TGF) were analyzed using RT-PCR. IL-6 and TNF protein were assessed immunohistochemically. In general, CDV infection resulted in induction of pro-inflammatory cytokines. In primary brain and DH 82 cells, IL-1, IL-6, and TNF were induced, and IL-1 and TNF but not IL-6 were upregulated in dermal fibroblasts. In contrast, in MDCK cells IL-1 and TNF expression was similar in infected and noninfected cells, whereas IL-6 was not produced in either condition. In addition, cytokine induction correlated to the degree of level of CDV production, and therefore cytopathic effects are presumed to be due to a direct virus-mediated or cytokine-mediated process. These findings suggest that pro-inflammatory cytokines, namely IL-1, IL-6, and TNF, which might play an important role in CDV pathogenesis, are induced in a cell-specific manner.
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PMID:Cell type-dependent cytokine expression after canine distemper virus infection. 1247 98

Necrotizing enterocolitis (NEC) seems to result from the inflammatory response of an immature intestine. Human milk is protective against NEC via an unknown mechanism. We hypothesized that specific factors found in human milk would decrease stimulated IL-8 secretion in intestinal epithelial cells. HT29-cl19A and Caco2 cells were compared with the fetal human primary intestinal epithelial cell line H4 and temperature-sensitive conditionally immortalized fetal human intestinal (tsFHI) cells. Cells were pretreated with transforming growth factor-beta (TGF-beta), erythropoietin (Epo), IL-10, or epidermal growth factor (EGF) at physiologic concentrations before stimulation with tumor necrosis factor-alpha (TNF-alpha) or IL-1beta, and then IL-8 was measured by ELISA. The fetal cells produced significantly more IL-8 when stimulated by TNF-alpha or IL-1beta. There were also differences in the pattern of alteration of IL-8 secretion by human milk factors. In HT29-cl19A cells, IL-10 inhibited TNF-alpha-stimulated IL-8 secretion by 52%, and EGF increased secretion by 144%. In H4 cells, TGF-beta1 and Epo inhibited TNF-alpha-stimulated IL-8 secretion to control levels, and EGF increased secretion by 29%. IL-1beta-stimulated IL-8 secretion was inhibited 25% by TGF-beta1 in Caco2 cells and in H4 cells was inhibited by TGF-beta1, Epo, and TGF-beta2. TsFHI cells confirmed H4 cell results. Fetal human enterocytes have an exaggerated IL-8 secretion in response to TNF-alpha and IL-1beta. TGF-beta and Epo decrease this stimulated IL-8 secretion, which may partially explain the protective effect of human milk in NEC.
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PMID:Modulation of human intestinal epithelial cell IL-8 secretion by human milk factors. 1259 89

Chronic lung disease (CLD) in premature newborns is associated with increased concentrations of inflammatory cytokines in tracheal aspirates (TA). We determined if polymorphisms of cytokine genes influence the risk of developing CLD by genotyping 178 mechanically ventilated very low birth weight (VLBW) infants for the tumor necrosis factor-alpha (TNF-alpha) -308 G/A, transforming growth factor-beta(1) (TGF-beta(1)) +915 G/C and monocyte chemoattractant protein-1 (MCP-1) -2518 A/G polymorphisms. Genomic DNA was isolated from TA and genotypes determined by restriction length polymorphism. There was no effect of any of these polymorphisms on the development of CLD (29 vs 23%, P=0.371, TNF-alpha -308 AA/AG vs TNF-alpha -308 GG; 23 vs 26%, P=0.681, MCP-1 -2518 GG/AG vs MCP-1 -215-8 AA; 24 vs 24%, P=0.978, TGF-beta(1) +915 CG vs TGF-beta(1) +915 GG). TA IL-8 and MCP-1 concentrations were not different between genotype groups. Infants with the TNF-alpha -308 A allele had increased risk of IVH (RR 2.07; 95% CI 1.02-4.18, P=0.041) and infants with the TGF-beta(1) +915 C allele were at greater risk of death (32 vs 9%, P=0.016). These data suggest that these polymorphisms do not play a significant role in determining risk for CLD in preterm infants, but may play a role in other complications in the neonatal period.
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PMID:The TNF-alpha -308, MCP-1 -2518 and TGF-beta1 +915 polymorphisms are not associated with the development of chronic lung disease in very low birth weight infants. 1294 79

Conventional pleurodesing agents often provoke acute pleural inflammation followed by fibrosis. The inflammation frequently causes pain and fever. Transforming growth factor (TGF)-beta is a pro-fibrotic but anti-inflammatory cytokine. Intrapleural TGF-beta2 administration produces effective pleurodesis in animals, but its effects on mesothelial cells are unknown. The authors hypothesised that, unlike conventional pleurodesing agents, TGF-beta2 can induce collagen synthesis without stimulating pleural inflammation. In the in vitro studies, TGF-beta2, talc and doxycycline were administered to rabbit mesothelial cells for 24 h. These agents were also injected intrapleurally in rabbits and the induced pleural fluids collected at 24 h. TGF-beta2 was as potent as talc and doxycycline in upregulating mesothelial cell collagen expression. Talc and doxycycline both induced significant increases in interleukin (IL)-8 production from mesothelial cells in vitro and in rabbit pleural fluids in vivo. TGF-beta2, however, did not stimulate mesothelial cell IL-8 release in vitro and induced a dose-dependent suppression of pleural fluid IL-8. Pleural fluid IL-8 levels correlated significantly with leukocyte and lactate dehydrogenase concentrations in the fluids. In summary, transforming growth factor-beta was a potent inducer of mesothelial cell collagen synthesis. Unlike talc and tetracycline, which provoked pleural inflammation, transforming growth factor-beta2 suppressed pleural inflammation in vivo. Transforming growth factor-beta2 can produce effective pleural fibrosis without necessitating acute pleural inflammation.
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PMID:Transforming growth factor-beta induces collagen synthesis without inducing IL-8 production in mesothelial cells. 1295 47

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