Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

High-quality monoclonal antibodies (mAbs) with specificity for relevant disease molecules can now be produced in abundance. Anti-tumour necrosis factor-alpha therapies have set a new standard for symptom control in rheumatoid arthritis, and blockade of tumour necrosis factor has the potential to protect joints from structural damage. Other targets for therapeutic antibodies include the cytokines interleukin (IL)-1, IL-6, IL-8, IL-15, IL-17 and IL-18. In addition, there is preliminary evidence for the clinical efficacy of both keliximab, a mAb targeting the T cell antigen CD4, and rituximab, a chimeric mAb against the B cell antigen CD20 and CTLA4-Ig, which blocks the CD28/B7 interaction. Phase III studies have yet to be undertaken for these novel biological agents, and it is unclear whether any of these agents will have true disease-modifying capabilities.
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PMID:Antibody therapy for rheumatoid arthritis. 1281 Feb

Analyses of cytokines mediating inflammatory reactions are key to understanding the etiopathology of various diseases. This study investigated differences in cytokine gene expression between pulps from healthy virgin teeth and from symptomatic vital teeth with severe caries lesions in a group of young, healthy individuals. The mRNA levels of IL-1alpha, IL-1beta, IL-6, IL-8, and IL-18 were measured concomitantly by quantitative real-time RT-PCR. IL-1alpha and IL-1beta were not expressed at significantly higher levels in symptomatic versus clinically healthy pulps, while the difference was significant for the other cytokines (log-rank test, P<0.05). A concordance test for independence revealed significant correlation between IL-1alpha and IL-1beta, and between IL-6, IL-8, and IL-18 mRNA levels (P<0.05). The cytokine-specific differences revealed a differential significance of gene expression in cytokine regulation. The hypothesis that increase of cytokine mRNA expression is part of host reaction in pulpitis was corroborated by our observation.
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PMID:Cytokine gene expression--part of host defence in pulpitis. 1284 7

Internalization of pathogens by phagocytic cells triggers the innate immune response, which in turn regulates the acquired response. Phagocytes express a variety of receptors that are involved in recognition of pathogens, including (1) pattern recognition receptors (PRR), which recognize conserved motifs, (2) complement receptors (CR), which recognize complement-opsonized pathogens, and (3) Fc receptors (FcR), which recognize antibody-opsonized pathogens. Recognition of microbes is accompanied by the induction of multiple cell processes, including the production of proinflammatory and anti-inflammatory cytokines and chemokines. The objective of the present experiments was to use probes to known avian proinflammatory and anti-inflammatory cytokines and TaqMan technology to ascertain levels of cytokine gene expression in avian heterophils following receptor-mediated phagocytosis of either nonopsonized Salmonella enteritidis (SE), serum-opsonized SE, or IgG-opsonized SE. Expression of interleukin-6 (IL-6) and IL-8, considered in mammals as a proinflammatory chemokine, were upregulated following exposure to the nonopsonized or the opsonized SE. However, mRNA expression for IL-18 and interferon-gamma (IFN-gamma) was downregulated, and the expression of mRNA for the anti-inflammatory cytokine transforming growth factor-beta4 (TGF-beta 4) was upregulated. Interestingly, IL-1beta mRNA expression was significantly upregulated in heterophils that phagocytized either the nonopsonized SE via PRRs or IgG-opsonized SE via FcRs, whereas serum-opsonized SE phagocytized by CRs induced a downregulation of IL-1beta mRNA. These results suggest that signaling interactions initiated by receptor recognition of the microbe surface differentially regulate the induction of inflammatory cytokines in avian heterophils.
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PMID:Differential regulation of cytokine gene expression by avian heterophils during receptor-mediated phagocytosis of opsonized and nonopsonized Salmonella enteritidis. 1285 58

One-week-old breast-fed miniature piglets were orally infected either with virulent LT2 strain or with a non-virulent SF1591 rough mutant of Salmonella Typhimurium for 1 d. Both microorganisms were cultivated from mesenteric lymph nodes but not from the blood of infected piglets. Interleukins (IL) 1 beta, 8, 18, tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) were quantified by ELISA in plasma and washes of a terminal part of the small bowel. In plasma, cytokines were mostly missing in non-infected piglets and either missing or low in infected piglets. In the gut of non-infected piglets, IL-1 beta, IL-8 and IL-18 were detected whereas TNF-alpha and IFN-gamma were mostly missing. IFN-gamma levels highly increased (p < 0.05) after infection with nonvirulent salmonellae. The variability of cytokine levels in the gut of suckling piglets is discussed.
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PMID:Systemic and local cytokine response of young piglets to oral infection with Salmonella enterica serotype Typhimurium. 1287 55

Infection of cells with influenza A virus results in cell death with apoptotic characteristics. Apoptosis is regarded as a non-inflammatory process. However, during influenza an inflammatory response occurs in the airway epithelium. An examination of this apparent paradox was made using influenza A virus infection of human nasal and bronchiolar epithelial cells. Some cytokine genes (IL-18, CCL2 and CCL5) were expressed constitutively in nasal cells but no cytokine was released. In bronchiolar cells, IL-1 beta, IL-6 and CXCL8 expression was constitutive, whilst CCL2 and CCL5 expression was upregulated following influenza virus infection. IL-6, CXCL8 and CCL5 were released but IL-1 beta and CCL2 were not. In bronchiolar cells, cell death was inhibited by the caspase-8 (Z-IETD-fmk) and pan-caspase (Z-VAD-fmk) inhibitors and these inhibitors enhanced expression of CCL5 and increased the levels of the three secreted cytokines significantly. Thus, the amount of each cytokine released from bronchiolar cells is reduced during cell death, implying that the observed inflammatory response in influenza would be greater if cell death did not occur. Reduced cytokine release is also associated with fragmentation of the Golgi body, as the caspase inhibitors also rescued influenza A virus-induced fragmentation of the Golgi ribbon.
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PMID:Influenza A virus-induced apoptosis in bronchiolar epithelial (NCI-H292) cells limits pro-inflammatory cytokine release. 1291 60

The aim of this study was to investigate potential differences in the local nasal immune response between bronchiolitis and upper respiratory tract infection induced by respiratory syncytial virus (RSV). Nasal brush samples were obtained from 14 infants with RSV bronchiolitis and from 8 infants with RSV upper respiratory tract infection. The samples were taken during infection (acute phase) and 2-4 weeks later (convalescent phase). Cytospin preparations were stained immunohistochemically for T cells, macrophages, and eosinophils. Staining also took place for intercellular adhesion molecule-1 (ICAM-1), T-helper 1 (Th1)-like (interleukin-12 [IL-12], interferon-gamma [IFN-gamma]), Th2-like (IL-4, IL-10), and proinflammatory cytokines (IL-6, IL-8, IL-18). During both RSV-induced bronchiolitis and upper respiratory tract infection, cellular inflammation was observed. This was characterised by an increase in the numbers of nasal macrophages, which tended to be higher in bronchiolitis than in upper respiratory tract infection. Numbers of T lymphocytes and ICAM-1 positive cells increased during both bronchiolitis and upper respiratory tract infection. There were no differences between numbers in the groups. Interestingly, a distinct nasal proinflammatory cytokine response was observed in RSV-induced bronchiolitis. This is characterised by an increase in the number of IL-18 positive cells. This increase is specific for bronchiolitis, as a similar increase could not be detected in RSV-induced upper respiratory tract infection. Numbers of IL-6 and IL-12 positive cells were higher in both bronchiolitis and upper respiratory tract infection, and there were no differences between the groups. By contrast, the number of IL-8, IFN-gamma, IL-4, and IL-10-positive cells remained constant. In conclusion, clear differences were found in nasal immune responses of children with RSV-induced upper respiratory tract infection or bronchiolitis. The induction of a strong IL-18 response was typical for bronchiolitis, as this could not be observed in RSV-induced upper respiratory tract infection, and could explain the eosinophilia that is observed frequently during bronchiolitis.
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PMID:RSV-induced bronchiolitis but not upper respiratory tract infection is accompanied by an increased nasal IL-18 response. 1293 5

Sepsis caused by gram-negative bacteria and that caused by gram-positive bacteria often manifest similar clinical features. We investigated plasma proinflammatory cytokine profiles in patients with sepsis due to gram-positive and gram-negative bacteria and studied the cytokine production and differential gene regulation of leukocytes stimulated ex vivo with Escherichia coli lipopolysaccharide or heat-killed Staphylococcus aureus. Concentrations of tumor necrosis factor alpha, interleukin 1 receptor antagonist (IL-1Ra), IL-8, IL-10, IL-18 binding protein, procalcitonin, and protein C in plasma did not differ between patients with sepsis due to gram-negative and gram-positive bacteria. However, plasma IL-1beta, IL-6, and IL-18 concentrations were significantly higher in patients with sepsis due to gram-positive bacteria. Ex vivo stimulation of whole blood with heat-killed S. aureus markedly increased IL-1beta and IL-18 levels more than E. coli lipopolysaccharide stimulation. Microarray analysis revealed at least 359 cross-validated probe sets (genes) significant at the P < 0.001 level whose expression discriminated among gram-negative-organism-stimulated, gram-positive-organism-stimulated, and unstimulated whole-blood leukocytes. The host inflammatory responses to gram-negative and gram-positive stimuli share some common response elements but also exhibit distinct patterns of cytokine appearance and leukocyte gene expression.
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PMID:Molecular characterization of the acute inflammatory response to infections with gram-negative versus gram-positive bacteria. 1450 May 2

Cytokines play a central role in the pathogenesis of allergic diseases and allergic inflammation. Therefore, an understanding of mechanisms which regulate production and function of cytokines is very important and may result in the development of more effective methods of treatment of allergic diseases. Recent studies have demonstrated that the induction of allergic inflammation requires genetic background and environmentak factors. The most important cytokines and chemokines are IL-4, IL-5, IL-3, IL-13, GM-CSF and TNF-alpha. Many other cytokines are responsible for the growth, maturity, migration activation and apoptosis of all cells involved in allergic inflammation, among them are IL-2, IL-5, IL-6, IL-9, MIP-1 alpha, RANTES, IL-8, IL-12, IL-18, IFN-alpha i gamma, TGF-beta, sIL-4, IL-1Ra. Recently it has been proven that IL-10 and other cytokines from the IL-10 family, and TGF-beta have anti-inflammatory properties in allergy.
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PMID:[Cytokines in allergic inflammation]. 1452 54

Heterophils, the principal avian polymorphonuclear leukocytes (PMNs) equivalent to the mammalian neutrophil, function as professional phagocytes against bacterial infections, mediate acute inflammation, and respond to cytokine stimulation to aid in regulation of innate host defenses. Interleukin-2 (IL-2) has been found to exercise an array of biological effects on other cell types besides T lymphocytes, including NK cells, B cells, monocytes, and neutrophils. In the present experiments, using real-time quantitative RT-PCR, we evaluated the role of rChIL-2 as a priming mediator controlling heterophil responses at the level of gene transcription by examining the expression of mRNA for pro-inflammatory (IL-1beta, IL-6, IL-8) and Th1 (IL-18 and IFN-gamma) cytokine genes following stimulation with phagocytosis agonists; i.e., opsonized and nonopsonized Salmonella enteritidis. Peripheral blood heterophils were isolated and incubated with rChIL-2 from transfected COS cells. rChIL-2 selectively primed the heterophils for an increase in transcription of the pro-inflammatory cytokine IL-8 and of the Th1 cytokine IL-18 induced by all three phagocytic agonists. Although rChIL-2 priming modulated the expression of specific cytokine mRNA in heterophils stimulated by different phagocytic agonists, the rChIL-2 by itself did not directly induce gene expression of either the pro-inflammatory or Th1 cytokines. We propose that rChIL-2 could be priming heterophils solely to function as more efficient innate effector cells to limit bacterial growth through the selective increase of IL-8 and IL-18 gene expression.
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PMID:Priming by recombinant chicken interleukin-2 induces selective expression of IL-8 and IL-18 mRNA in chicken heterophils during receptor-mediated phagocytosis of opsonized and nonopsonized Salmonella enterica serovar enteritidis. 1459 63

The reaction of the intestinal immune system to intestinal bacteria shows striking differences between various bacterial strains. Whereas Klebsiella pneumoniae induces a fierce proinflammatory reaction, the probiotic strain Lactobacillus rhamnosus has clear anti-inflammatory effect in gastrointestinal disease and allergy. The molecular basis for this dichotomy is poorly understood but is likely to involve different modulation of antigen-presenting dendritic cells (DC) by L. rhamnosus and K. pneumoniae. Hence we evaluated phenotypic and functional characteristics of DC matured in the presence of L. rhamnosus and K. pneumoniae. Monocyte-derived immature DC were cultured in the presence of live bacteria to obtain mature DC. Both micro-organisms induced maturation of immature DC as shown by CD83 and CD86 expression, but receptors involved in activation of Th1 cells were expressed predominantly on DC exposed to K. pneumoniae. In contrast to K. pneumoniae, maturation with L. rhamnosus resulted in lower TNF-alpha, IL-6, and IL-8 production by immature DC and lower IL-12 and IL-18 production by mature DC. Moreover, L. rhamnosus led to the development of T cells without a typical Th phenotype whereas K. pneumoniae induced a Th1 immune response, dependent mainly on IL-12 production. Thus our results strongly support the concept that differential modulation of DC explains the differences in the immune response to various bacterial strains and indicates that K. pneumoniae induces Th1 immune responses via DC.
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PMID:Dichotomy between Lactobacillus rhamnosus and Klebsiella pneumoniae on dendritic cell phenotype and function. 1467 29


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