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)

The authors studied the inflammation's factors of the lung in six asthmatic children in BAL liquid. Were monitored either the cells either the inflammation's mediators as PCF--albumin--PGE2--PG1 alpha--Tx beta 2--PAF--LT beta 4 and the interleukines IL1 alpha--IL-1 beta--IL-6--IL-8. In the BAL liquid was observed the macrophagic non epiteliomorphic and lymphocytic preminence. The mediators of inflammation were all increased in particular IL-1 beta--IL-6--IL-8. The cultural exams were negatives in 80% of children.
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PMID:[The correlations between chemical mediators and interleukins in the bronchoalveolar lavage fluid in 6 asthmatic children]. 832 21

Our recent studies indicate that lipocortin 1 (LC1), a putative second messenger protein for the anti-inflammatory steroids in peripheral tissues, may also contribute to the regulatory actions of the glucocorticoids on the hypothalamo-pituitary-adrenal axis. In the present study we have used in vitro and in vivo models to compare the effects of adrenalectomy, LC1 and dexamethasone on the cytokine-induced secretion of the 41-amino acid corticotrophin releasing factor (CRF-41) and arginine vasopressin (AVP) by the rat hypothalamus. In addition, western blot analysis was used to examine the influence of dexamethasone on the expression of LC1 in the hypothalamus. In vitro, interleukins- (IL-) 1 alpha (100 and 200 pg/ml), 1 beta (0.5 and 1.0 ng/ml) and 8 (0.25-1.0 ng/ml) readily initiated the release of CRF-41 and AVP from hypothalami removed from intact rats. IL-6 (10 and 20 ng/ml) was also an effective CRF-41 secretagogue but, unlike the other interleukins tested, it was ineffective with regard to AVP. Adrenalectomy 7-14 days prior to autopsy increased significantly (p < 0.01) the magnitude of the CRF-41 responses to IL-1 alpha, IL-1 beta and IL-6 but not to IL-8. In contrast however, while hypothalamic tissue from adrenalectomized rats, unlike that from intact animals, responded to IL-6 (5-20 ng/ml) with a pronounced hypersecretion of AVP, the AVP responses to IL-1 alpha and IL-1 beta were largely unaffected by adrenalectomy as too were those to IL-8. The marked increases in CRF-41 and AVP release from hypothalami from adrenalectomized rats initiated in vitro by IL1 alpha, IL-1 beta, IL-6 and IL-8 were readily overcome by preincubation of the tissue with dexamethasone (10(-7) M). In addition, the steroid caused 'externalization' of two species of immunoreactive (ir-) LC1 (37 and 58 kDa) by the hypothalamic cells but failed to influence the total LC1 content of the tissue. The inhibitory effects of dexamethasone on the cytokine-induced release of CRF-41 in vitro were mimicked by LC1 (10 ng/ml) which alone had no effect on the basal release of the peptide. However, unlike dexamethasone, LC1 failed to influence the concomitant release of AVP from the hypothalamic tissue elicited by IL1 alpha, IL-1 beta or IL-8 and potentiated that evoked by IL-6.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Modulation of the hypothalamo-pituitary-adrenocortical responses to cytokines in the rat by lipocortin 1 and glucocorticoids: a role for lipocortin 1 in the feedback inhibition of CRF-41 release? 841 17

The alcoholic liver cirrhosis usually causes overall immunological changes which might be attributed to either the hepatic disease itself, to ethanol action and/or to malnourishment of the patient. These immune abnormalities comprise both cellular and humoral immunity, consisting of increased immunoglobulin levels, depressed late-skin response to antigens, lowered proliferative response of lymphocytes to mitogens, lower plasma levels of complement proteins (C3 and C4) and by either lower (IL2 and gamma IF) or increased (IL1, TNF, IL6 and IL8) cytokine levels. Parallel to the systemic immune suppression found in most patients, there is also a concomitant local, genetically based, immune stimulation at the liver level which leads to hepatic self-aggression. The systemic immune-suppression could be responsible for periodical infections or neoplasia found in these patients. The possible factors for the immune exhaustion are: a) lower hepatic clearance of toxins and/or bacteria; b) lower hepatic synthesis of complement components; c) cytokines (IL2 and gamma IF) deficiencies, and d) deficiencies of nutrients related to the antioxidant and/or immune defense mechanisms. The immune stimulation of the liver self aggression is characterized by the preferential migration of cytotoxic T cell and neutrophils to the liver, following stimulatory factors such as Mallory bodies, acetaldehyde and/or antibodies. Moreover, the local increase of cytokines (IL1, TNF, IL6 and IL8) levels would be liable for the local phagocyte chemotaxy (IL8) or part of liver injury (TNF) eased by the lower antioxidant defense of the cirrhotic liver.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immunologic changes in alcoholic liver cirrhosis]. 854 Aug 5

Vascular endothelial cells (EC) play a key role in viral tropism in vivo. Since conflicting reports have been published on the capability of HIV to infect EC in vitro, we analyzed some factors potentially capable of influencing the susceptibility of human umbilical vein endothelial cells (HUVEC) to HIV-1. Both primary cultures and differentiated immortalized HUVEC lines were used. HUVEC were negative for the expression of CD4, but weakly CD26- and galactosylceramide-positive. Although binding of HIV to EC was substantial, the virus was apparently incapable of replicating in nonproliferating cultures. In resting cultures, the content of cell-associated HIV disappeared 4-6 days after infection without production of p24 and infectious progency. In contrast, infection of proliferating EC cultures led to the transient release of p24 and infectious virus (10(2.5)-10(3.5) SFU/ml) peaking 2-6 days postinfection. Antibody neutralization of cytokines that may be produced by EC (IL1, IL6, IL8, TNF, IFN-beta) failed to modify virus adsorption and replication, whereas treatment with IL1-beta plus TNF-alpha stimulated both virus binding and virus release. As seen by gag polymerase chain reaction (PCR), the viral genome persisted up to 15 days in untreated EC cultures, but over 20 days in cultures exposed to IL1-beta plus TNF-alpha. This study shows that: (a) CD4-negative HUVEC are capable of binding substantial amounts of HIV-1; (b) binding is enhanced by proinflammatory cytokines; (c) the establishment of productive infection is favored by cell proliferation; and (d) exposure to IL1-beta plus TNF-alpha enhances virus replication.
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PMID:Productive HIV-1 infection of human vascular endothelial cells requires cell proliferation and is stimulated by combined treatment with interleukin-1 beta plus tumor necrosis factor-alpha. 863 3

The exact changes in cytokine production and clinical implications of the increased cytokine levels following operative trauma remain unclear. In this study, systemic production of a spectrum of cytokines, including IL1 alpha, IL1 beta, IL6, IL8, IL10, and IFN gamma, was examined in patients undergoing minor elective operative trauma. The levels of IL1 receptor antagonist (ra) and IL6 soluble receptor (sR) were also determined. Although there were no changes in IL1 alpha and IL1 beta plasma levels during the entire observation period, there was a significant rise in IL1 ra level in all patients between postoperative day 1 and postoperative day 14. A significant increase in the IL6 plasma level was seen on days 1, 3, and 7 after surgery and an increase in the IL6 sR level was observed on postoperative days 10 and 14. Interestingly, the IL8 plasma values had risen significantly on days 1 and 3 following the operation. In some patients, an elevation in IL10 plasma level was noted on days 1 and 3 postsurgery. Results demonstrated that even a minor surgical procedure such as cholecystectomy with uneventful wound healing was followed by an appearance in the blood circulation of significant levels of cytokines between day 1 and day 14 after surgery. These observations point to the necessity of searching for methods of down-regulating the systemic cytokine effects after surgical trauma for the routine postoperative management.
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PMID:Blood cytokine levels rise even after minor surgical trauma. 873 59

Fibrosing colonopathy is a recently described complication of cystic fibrosis, of unknown aetiology but possibly related to treatment with high-dose pancreatic enzyme supplements. We have used a whole gut perfusion technique to study subclinical gut inflammation in cystic fibrosis patients; concentrations of haemoglobin, IgG, albumin, alpha-1-antitrypsin, granulocyte elastase, IL1 beta, and IL8 were measured in whole gut lavage fluid: 23 tests were performed in 17 children with cystic fibrosis (20 elective tests, three lavages to treat distal intestinal obstruction syndrome (DIOS)). None has had fibrosing or haemorrhagic colitis. There were 12 tests in control children with constipation or precolonoscopy. Moderately abnormal results were obtained for many of the parameters studied, in specimens from all the cystic fibrosis children; however there were no significant differences between tests on high-dose and low-dose enzyme supplements of the same brand in the five children who had duplicate tests performed electively. The lavage fluid specimens from two cystic fibrosis children were strikingly abnormal in all tests apart from haemoglobin and alpha-1-antitrypsin. These were two of the three children with DIOS, and were also the only cases in the series taking Nutrizym 22. These data suggest that the majority of cystic fibrosis children, including those on high-dose enzyme supplements, do not have clinically significant colitis, but that there is subclinical mucosal inflammation in a minority (two of 17 in this series), for which DIOS and/or Nutrizym 22 treatment may be risk factors. Alternatively, inflammation and dysmotility in the proximal colon may be directly produced by a drug or other agent, producing a clinical syndrome indistinguishable from DIOS. Tests for indices of inflammation in gut lavage fluid offer a new approach to the detection and measurement of iatrogenic intestinal and colonic injury.
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PMID:Direct assessment of gastrointestinal inflammation and mucosal immunity in children with cystic fibrosis. 886 80

Growth-regulated gene product/cytokine-induced neutrophil chemoattractant (GRO/CINC)-1 is a rat chemokine with structural and functional homology to human IL-8. Chemokines are a family of cytokines whose participation in nasal inflammation in vivo remains to be established. Using ELISA and RT-PCR, we investigated the production and gene expression of GRO/CINC-1 in rat nasal lavage and mucosa in vivo. GRO/CINC-1 in nasal lavage was produced by stimulation of LPS, ConA and IL1-beta. GRO/CINC-1 showed time- and dose-dependent production under all stimulants, but was more slowly induced by IL-1 beta. The steady-peak of the GRO/CINC-1 production remained at 3 h with LPS or ConA exposure, whereas it lasted 4 h or more after IL-1 beta exposure. At the time of peak production of GRO/CINC-1, we found that mRNA for the GRO/CINC-1 was induced in the nasal mucosa. The mRNA of the related inflammatory cytokines TNF-alpha and IFN-gamma were also expressed in nasal mucosa with stimulation of these reagents. Thus, this study revealed that exposure to bacterial endotoxin, mitogenic reagent and also IL-1 beta induced the production and gene expression of the neutrophil chemoattractant GRO/CINC-1 in rat nasal mucosa in vivo. This investigation of the characteristics of IL-8 family in nasal mucosa using rat models has extended the functional concept of cytokines in the inflammatory condition of nasal cavity in humans.
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PMID:Production and gene expression of IL-8-like cytokine GRO/CINC-1 in rat nasal mucosa. 903 93

We have examined in detail the activities of IL-13 on monokine production in vitro and compared its effects with those of IL-10 and IFN-gamma. IL-13 and IL-10 show qualitatively and quantitatively similar activities on cytokine production by monocytes when administered simultaneously with LPS i.e. inhibition of IL-1, IL-6 and TNF-alpha, up-regulation of IL1-ra. However when either LPS and IFN-gamma or fixed S. aureus Cowan (SAC) are used to activate monocytes, IL-10 is a much more potent inhibitor of TNF-alpha production than is IL-13. IL-10 is also an extremely potent inhibitor of IL-12 (p70) production when given with either SAC or LPS, while IL-13 has little effect. Indeed, IL-13 actually increases SAC-induced IL-12 production. When IL-13 is administered prior to the LPS stimulation, its modulation of cytokine production is drastically different. Production of IL-12, MCP-1, TNF-alpha and to a lesser extent IL-6 induced by LPS is now "primed", whereas that of IL-1, IL-8, and IL-10 is still inhibited. IL-10 does not show this "priming" effect, and is a dominant inhibitor of IL-13. The initial IL-13 priming effect is not however due to an inhibition of endogenous IL-10 production; nor is it due to inhibition of PGE2 production. The priming effect of IL-13 on IL-12 production is additive with that of IFN-gamma, and is partly independent of IFN-gamma. The earliest event in IL-13 priming so far noted is an increase in TNF-alpha mRNA production at 1-2 hours. IL-13 priming of IL-12 production can be completely abolished by anti-TNF-alpha antibodies suggesting that IL-13 may be priming via increased TNF-alpha expression, although merely substituting TNF-alpha for IL-13 does not reproduce the priming effect. IL-13 is a thus a more subtle immune regulator than IL-10 or IFN-gamma. When administered with LPS or SAC, it dampens the resulting inflammatory response, though in a more selective way than IL-10. In contrast, when it is added before an inflammatory signal, it primes an immunostimulatory monokine secretion profile resembling that of IFN-gamma, but without the proinflammatory IL-1 component. Early in response to an inflammatory stimulus, IL-13 may thus play an essentially anti-inflammatory role, switching to a primarily immunostimulatory role in the case of an ongoing infection.
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PMID:Interleukin-13 effects on activated monocytes lead to novel cytokine secretion profiles intermediate between those induced by interleukin-10 and by interferon-gamma. 926 68

IL4 has been shown to differentially modulate HIV1 replication in primary cells of the monocyte/macrophage lineage. Its effects on chronic HIV1 infection, however, are unknown. To address IL4-mediated effects on promonocytic cells chronically infected with HIV1, U1 cells were incubated in the presence or absence of IL4 together with cytokines that are known to induce both HIV1 and IL8 expression. IL4 enhanced IL1 beta-induced HIV1 and IL8 expression in promonocytic U1 cells, whereas it suppressed their expression induced by cytokines IL6, GM-CSF and to a small extent, TNF alpha. IL4 suppressed IFN gamma-induced IL8 production with increasing IL4 concentration, while HIV1 p24 core antigen production was suppressed at low IL4 input (0.1 and 1 U/ml) but was substantially enhanced at a high IL4 input concentration (10 U/ml). Results showed that the immunosuppressive cytokine IL4 can behave variably in modulating HIV1 and IL8 expression, depending on both the inducing cytokine and the input concentration of IL4.
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PMID:Interleukin-4 regulation of cytokine-induced HIV1 and interleukin-8 expression in promonocytic U1 cells is concentration- and cytokine-dependent. 956 61

A large number of clinical studies has described procalcitonin (ProCT) as a marker of bacterial infection and a good predictor of disease severity and antibiotherapy efficacy. Nevertheless, the mechanism of ProCT synthesis remains unclear. The aim of this study was to demonstrate potential ProCT production by peripheral blood mononuclear cells as is the case for cytokines involved in sepsis. In a whole blood model, LPS (10 micrograms/ml) stimulation on blood samples from healthy volunteers (n = 14) was tested. Early (TNF-alpha and IL1-beta) and late (IL-6 and IL-8) cytokines were produced in large amounts in contrast to the absence of ProCT. Additional experiments with nitric oxide or detection of intra-cellular ProCT (cell lysis, flow cytometry) had negative results. It was concluded that ProCT is not produced in this model. Data are still needed to investigate the cellular origin of ProCT in order to better define its clinical usefulness.
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PMID:Procalcitonin is not produced by circulating blood cells. 1002 4


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