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

Human bronchial epithelial cells are involved in airway immune mechanisms through secretion of cytokines and through cell-cell contacts with immunocompetent cells. The aim of our study was to assess the ability of interferon (IFN) alpha and gamma alone and in combination to modulate human bronchial epithelial cell (HBECs) release of the inflammatory cytokines IL-8 and IL-6 and fibronectin and to induce the surface expression of HLA-DR and ICAM-1 molecules involved in immune interactions with other cells. HBECs spontaneously secreted a limited amount of IL-8, which was significantly increased by IFN gamma. IFN alpha inhibited IFN gamma stimulated IL-8 secretion in a concentration-dependent manner. Further, IFN gamma induced IL-6 and fibronectin secretion, and this was also inhibited by IFN alpha. The expression of HLA-DR antigens was significantly increased by IFN gamma and partially inhibited by co-stimulation with IFN alpha. In contrast, IFN gamma also induced ICAM-1 expression by HBECs but co-stimulation with IFN alpha had no significant effect on the expression of this surface antigen. IFN alpha modulation of HBEC functions does not seem to be restricted to IFN gamma stimulation since either stimulatory or inhibitory effects of INF alpha on IL-8 production have been found in pilot experiments using IL-1 beta, TNF alpha, and TGF beta as stimuli. In summary, IFN-gamma induces a number of responses in HBECs including increased secretion of IL-6, IL-8 and fibronectin and increased expression of HLA-DR and ICAM-1. IFN alpha can inhibit all these except expression of ICAM-1 which is unaffected. IFN alpha can also interact with other inflammatory cytokines, but whether the effects are inhibitory or augmentive depends on the cytokines.
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PMID:Effects of interferons alpha and gamma on cytokine production and phenotypic pattern of human bronchial epithelial cells. 1098 52

Psoriasis is currently considered to be an inflammatory disease of the skin mediated by T-lymphocytes. The key role in the pathogenesis of psoriasis is played by IL-8 which together with INF-gamma have a mitogenic effect on keratinocytes and trigger their hyperproliferation and activation of neutrofile leucocytes as well as the inflammatory reaction. The skin afflicted with psoriatic lesions contains 100-times increased expression of active IL-8. Its most significant source is probably represented by keratinocytes, but it is produced also by endothelial cells, fibroblasts, T-lymphocytes, polymorphonuclear leucocytes, fibroblasts, Langerhans cells, macrophages. The revealed pathogenetic coincidences render new prospective possibilities in the treatment of psoriasis.
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PMID:[New findings on the pathogenesis of psoriasis]. 1118 60

This study was designed to investigate subacute effects of long-term exposure of both healthy and chronically inflamed human respiratory mucosa to ozone. Functional and metabolic effects on ciliary beat frequency (CBF), release of interleukin 8 (IL-8), interleukin 4 (IL-4), and gamma interferon (g-INF), as well as cellular viability and cytotoxicity, were monitored. Cell cultures of 60 specimens (healthy mucosa: n = 30, inflamed mucosa: n = 30) were exposed to synthetic air and to ozone-enriched synthetic air in different concentrations of 100, 500, and 1000 micrograms/m3. Continuous expositions were performed using an air/liquid interface cell culture technique for a period of 4 weeks. CBF was monitored using video-interference contrast microscopy and cytokine release was quantified by enzyme immunoassays. Cellular viability and cytotoxicity were controlled by measuring lactate dehydrogenase activity, cytosolic activity of esterases, and by staining of nuclear DNA. Synthetic air had no influence on CBF during the 4 weeks of exposure. IL-8 release was continuously diminished in unaffected and in chronically inflamed mucosa. Within the first week of continuous exposure with any ozone concentration neither CBF nor release of IL-8 were affected in healthy or in inflamed mucosa. During the second and the following weeks of exposure CBF and the release of IL-8 were reduced in both tissues. Release of IL-4 or g-INF were not detectable at any time during the 4 weeks of ozone exposure. At higher ozone concentrations of 500 and 1000 micrograms/m3 there was an increase of cytotoxicity which was greater in chronically inflamed than in healthy mucosa. In conclusion, ozone had no measurable effect on those parameters measured in human upper respiratory epithelium after one week of in vitro exposure to different concentrations, but did after longer periods of exposure. Chronically inflamed mucosa had a tendency toward a higher susceptibility to intermediate and high concentrations of ozone that did not reach a level of statistical significance under the conditions used in this study.
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PMID:Subacute effects of ozone exposure on cultivated human respiratory mucosa. 1119 18

Although some previous studies have indicated the possibility of immunosuppression withdrawal in clinical liver transplantation, the mechanism of graft acceptance is not clear. The aim of this study is to elucidate the alloreactivity against the donor and intragraft cytokine profiles in living donor liver transplant (LDLT) recipients with graft acceptance. In October 1999, we had 23 patients who survived without immunosuppression after LDLT with a median drug-free period of 25 months (range: 3-69 months). They consisted of six patients who were electively weaned by an elective weaning protocol and 17 either forcibly or accidentally weaned patients due to various causes but mainly due to infection. We evaluated the alloreactivity against the donor in these patients by a mixed lymphocyte reaction and intragraft cytokine profiles by real-time reverse transcriptase-polymerase chain reaction. The development of donor-specific hyporeactivity was observed in the patients with graft acceptance. The cytokine pattern in the supernatant of the culture medium revealed a down regulation of T helper (Th) 1 cytokine INF gamma against the donor while no significant difference was seen in Th2 cytokine IL-10. Regarding the intragraft cytokine profiles, we could find no amplification of Thl cytokines (IL-2, INF y) and IL-4 while some of the patients revealed a gene expression of IL-10 with no significant difference from that of the normal, untransplanted liver specimen. In addition, no difference was observed in any other cytokines (IL-1beta, IL-8, IL-15, TNFalpha) compared with those of the normal controls. We propose that the down regulation of Th1 cytokine is one possible mechanism of graft acceptance in LDLT recipients.
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PMID:Analysis of alloreactivity and intragraft cytokine profiles in living donor liver transplant recipients with graft acceptance. 1131 71

Chemokines constitute a group of cytokines with strong chemotactic activity towards different populations of leukocytes, playing significant role in the pathogenesis of inflammatory responses. The chemokines of the alpha subfamily act mainly on neutrophiles, while beta subfamily chemokines attract primarily monocytes and lymphocytes. Research conducted within the last few years suggests chemokines to be the main factors responsible for the attraction of leukocytes to the cerebrospinal fluid (CSF) in the course of both bacterial and viral meningitis. In cerebrospinal fluid from patients with meningitis of different etiologies significant concentrations of both alpha and beta chemokines were observed, which tended to decrease after the introduction of the treatment, with the relationship to the clinical improvement. It was also confirmed in in vitro experiments that the chemotactic properties of the inflammatory CSF mainly depend on the presence of chemokines. The most important chemokines in the pathophysiology of the meningitis in humans are probably interleukin 8 (IL-8), monocyte chemoattractant protein (MCP-1) and INF-gamma inducible protein (IP-10). They seem to be responsible for the attraction to the cns of, respectively, neutrophiles, monocytes and activated T lymphocytes. Differences between the chemokine profiles observed in meningitides of different etiologies are to some degree relevant to coexisting differences in type and extent of pleocytosis. In future, measurements of concentrations of certain chemokines may become of some importance in diagnostics of meningitis and monitoring its clinical course.
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PMID:[Chemokines in meningitis of different etiologies]. 1132 May 78

The essential in pathogenesis of RA is induction of incorrect immunological response against synovial and connective tissue antigens, which depends of CD4+ T-cells activation by specific antigen. This stimulation leads to releasing Th1 lymphokines. The most important cytokine is TNF-alpha. An increased level of TNF-alpha, IL-1, IL-6, GM-CSF, IL-8 was observed in patients with RA. PDGF, FGF, TGF, C-X-C a chemokines (IL-GRO-alpha, ENA78) and CCb chemokines (RANTES, MCP1 MIP1 alpha) are also involved in synovial hyperplasia in RA. During a pregnancy a clinical improvement in women with RA is frequent. The reason of this fact is probably connected with Th2 predominance (IL-4, IL-10) caused by presence of fetal tissues. Specific, cell-mediated immunity is suppressed and changed to Th2 by progesterone and PGE2. During a pregnancy a higher sensitivity of lymphocytes to progesterone was found. Progesterone stimulates T cells to PIBF production, which decreases NK activity. Th2 cytokines (Il-6, IL-10, IL-13, TGF) are expressed on decidua and inhibit secretion of Th1 cytokines (IL-2, INF gamma, TNF-alpha, IL-1 alpha, IL-1 beta). Immunosuppression caused by pregnancy probably decreases inflammatory and destructive reactions in tissues women with RA. The first attack of this disease frequently observed during puerperium is connected with a high level of prolactin and a low of estrogens, which causes a increased release of IL-2 and has a main influence on initiation and increasing of inflammatory process in RA.
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PMID:[Current opinions on immunological processes in rheumatoid arthritis during pregnancy]. 1150 69

In all living species, the first line of defence against microbial aggressions is constituted by innate immunity. During Evolution, it appears in invertebrates and plants, long before adaptive immunity, which appears in vertebrate. Adaptive immunity induces acquired resistance against microorganisms through random somatic rearrangements of genes encoding immunoglobulins and T cell receptors, thus generating a high level of diversity of receptors (>10(9)) in response to microbial aggressions. Acquired resistance is not vertically transmitted and reflects the "infectious history" of every individual. In contrast, innate immunity relies on recognition of antigens by a small number of weakly specific receptors (>10(2)) designated Pattern-Recognition Receptors (PRR) and is vertically transmitted by germinal cells. The PRR are expressed on macrophages dendritic cells and B lymphocytes and recognize antigenic structures highly conserved in the living world, termed Pathogen-Associated Molecular Patterns (PAMP), as lipopolysaccharides peptidoglycanes and lipoteichoic acids. PRR are secreted (complement, lectins), or expressed at the cell surface of cells to induce endocytosis or signaling (Toll-like receptors or TLRs). The recognition of antigens induces an immediate inflammatory response and triggers adaptive immunity. Among secreted PRR, the system of complement plays a major role in the immediate inflammatory response, controlling infections by its major role in opsonization, chemotactism and activation of leucocytes. TLRs induce the inflammatory response against microorganisms through NF-kB, a cytoplasmic factor controlling transcription of many genes, including cytokines (TNF, INF, IL-1, IL-2, IL-8, IL-12.) and defensines. So, within few minutes following microbial aggression, the inflammatory response is rapidly triggered to destroy infectious agents and to generate a long-term memory against pathogens.
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PMID:[Bacterial aggression]. 1284 61

Expression of immune modulating mediators in human Islets of Langerhans could have important implications for development of autoimmunity in type 1 diabetes and influence the outcome of clinical islet transplantation. Islets obtained from five donors were analyzed at various times after isolation using cDNA array technology. The Atlas Human Cytokine/Receptor and Hematology/Immunology nylon membranes representing 268 genes and 406, respectively, were used and the relative expression of each gene analyzed. Of the 51 gene products identified, high mRNA expression of MCP-1, MIF, VEGF, and thymosin beta-10 was detected in all islet samples. IL-8, IL-1-beta, IL-5R, and INF-gamma antagonist were expressed in islets cultured for 2 days. IL-2R was expressed in islets cultured for more than 6 days. In conclusion, several inflammatory mediators were expressed in isolated islets, particularly at an early stage after isolation, indicating that a few days of culture could be beneficial for the outcome of islet transplantation.
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PMID:Inflammatory mediators expressed in human islets of Langerhans: implications for islet transplantation. 1291 74

Recent studies have evaluated the cytokine network involved in the local immune response to tumors. In addition to infiltrating inflammatory cells, tumors also produce cytokines and growth factors that may alter tumor growth and tumor immunogenicity. Ninety-one samples of NSCLC were used in this study. We measured the expression of VEGF, TNF-alpha, TGF-beta, IL-6, IL-8, IL-12, INF-gamma, and MCP-1 in NSCLC tissues, by ELISA. The expression of IL-6 and IL-8 were significantly higher in squamous cell carcinoma than in adenocarcinoma (p=0.016 and p<0.001, respectively). The expression of TGF-beta, MCP-1 and IL-8 were significantly higher in pulmonary metastasis positive than negative cases (p=0.002, p=0.001, and p=0.008, respectively). In multivariate logistic regression analysis, the expression of TGF-beta was an independent risk factor for the occurrence of pulmonary metastasis (p=0.008, 95% CI=1.002-1.011). We confirmed that tumor infiltrating stromal cells were major sources of TGF-beta by immunohistochemical analysis. The expression of VEGF and IL-8 were significantly higher in cases with central necrosis (p=0.006 and p=0.011, respectively). We speculated that TGF-beta expression in tumor infiltrating stromal cells may regulate the occurrence of spontaneous pulmonary metastasis in NSCLC. (Ann Thorac Cardiovasc Surg 2003; 9: 295-300)
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PMID:Significance of expression of TGF-beta in pulmonary metastasis in non-small cell lung cancer tissues. 1467 25

Tumor necrosis factor (TNF-alpha) in conjunction with interferon-gamma (IFN-gamma) plays an important role in lymphocyte recruitment and granuloma formation in mycobacterial diseases. Lepromatous leprosy infections are typically associated with low to absent T cell responses and the absence of INF-gamma secretion. Chemokines such as IL-8, MCP-1, and MIP-1beta, have also been shown to recruit neutrophils and lymphocytes to the site of mycobacterial infections. We have studied IL-8 expression in relation to TNF-alpha and TGF-beta in monocytes from lepromatous patients (LL) as compared with healthy endemic controls. In endemic controls, no spontaneous expression of IL-8, TNF-alpha, and TGF-beta was observed, but BCG and M. leprae induced activation of all three cytokines. Lepromatous leprosy monocytes spontaneously expressed high levels of IL-8 and TGF-beta but negligible levels of TNF-alpha. A further increase in IL-8 secretion or gene expression by BCG or M. leprae was not significant. BCG, but not M. leprae, was able to stimulate TNF-alpha activation in lepromatous leprosy subjects. TGF-beta responses in LL were parallel to those of IL-8. This suggests a vigorous and active ongoing IL-8 response in lepromatous disease that is independent of TNF-alpha activation. Therefore, in the absence of IFN-gamma and TNF-alpha activation, IL-8 may assume a pivotal role in cell recruitment in leprosy patients with disseminated mycobacterial infections.
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PMID:Leprosy patients with lepromatous disease have an up-regulated IL-8 response that is unlinked to TNF-alpha responses. 1521 17


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