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)

The present study aimed to examine the cytokine expression pattern of human oral mucosa-derived keratinocytes at the protein and RNA level. The mRNA expression was measured by a RT-PCR method and the protein production was determined by an ELISA technique. In freshly isolated oral keratinocytes, IL-1alpha (interleukin 1alpha), IL-6, IL-8, transforming growth factor beta, tumor necrosis factor alpha and basic fibroblast growth factor were detectable at the protein and mRNA level, whereas platelet-derived growth factor, acidic fibroblast growth factor and transforming growth factor alpha were found only at the mRNA level. There were no detectable signals of IL-2 and IL-4. The cytokine production at the protein level was independent of prior stimulation with phorbol myristate acetate. Our results show that human oral keratinocytes - under nonpathological conditions - produce a cytokine pattern quite similar to that of epidermal keratinocytes, which may have implications for further functional studies.
 ...
PMID:Cytokine expression of human oral keratinocytes. 1009 1

Using two-color flow cytometry, we measured intracellular expression of interleukin-1 alpha (IL-1 alpha), IL-2, IL-4, IL-6, IL-8, interferon gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) in tonsillar mononuclear cells freshly isolated and stimulated by phorbol myristate acetate (PMA) and ionomycin. In freshly isolated tonsillar mononuclear cells, IL-1 alpha was produced in 0.39% of CD3 cells, 0.48% of CD4 cells, 0.66% of CD19 and 11.2% of CD14 cells; TNF-alpha was found in 5.4% of CD14 cells. After 8-hour culture without any mitogens, IL-4, IL-8, TNF-alpha and IL-1 alpha were detected in 2.1%, 0.8%, 0.55%, and 0.42% of tonsillar mononuclear cells, respectively. Flow cytometric detection of intracellular cytokines in tonsillar mononuclear cells stimulated with PMA and ionomycin revealed that CD3 cells produced IL-1 alpha, IL-2, IL-4, IL-8, IFN-gamma and TNF-alpha, and CD19 cells produced IL-1 alpha, IL-6, IL-8 and TFN-alpha. In CD3 cells, the number of cells producing IL-2 and TNF-alpha were significantly higher than those expressing other cytokines; and the number of cells producing IFN-gamma and IL-8 were significantly higher than those expressing IL-4 and IL-1 alpha. In CD19 cells, the number of cells producing IL-6 and TNF-alpha were significantly higher than those of IL-8 and IL-1 alpha; and the number of cells producing IL-8 was significantly higher than that of IL-1 alpha. There was no difference in the number of CD3 and CD19 cells producing any cytokine between the adult recurrent tonsillitis group and adult obstructive sleep apnea syndrome group. However, the number of CD3 cells producing IL-2 or TNF-alpha and CD19 cells producing IL-1 alpha, IL-6 or TNF-alpha were significantly lower in children than that of adults (p < 0.05). These findings indicate that the cytokine production in tonsillar mononuclear cells is heterogenous according to the subset and activation and that flow cytometric analysis of intracellular cytokines is a useful means to investigate the pathophysiological role of cytokines in the tonsils.
 ...
PMID:[A study of cytokine in palatine tonsil--flow cytometric analysis of cytokine production in tonsillar mononuclear cells]. 1019 28

Differential cDNA displays between hepatocellular carcinoma and adjacent non-malignant tissues have previously detected a PCR product, hIRH (human intercrine reduced in hepatomas), equivalent to SDF1alpha/PBSF whose mRNA was lost from human hepatocellular carcinoma and other malignant and pre-malignant samples and malignant cell lines. There are no reports to date of the mRNA status of the receptor for hIRH/SDF1alpha/PBSF, CXCR4 in malignant tissues. We report here that there is a reduction in the mRNA expression of CXCR4 in hepatocellular carcinoma as estimated by Northern blot and RT-PCR and compared to the adjacent non-malignant tissue. The average (mean SD) tumor/normal ratio for CXCR4 mRNA expression, determined by RT-PCR, was 0.65 0.36 in 10 pairs of hepatocellular carcinomas. There was no consistent loss of CXCR4 mRNA expression in a range of malignant cell lines. The 3'-non-coding region of hIRH, had typical early response gene element sequences. Despite the presence of these 3'-elements there was no induction of hIRH gene expression in human lung carcinoma A549 cells by tumor necrosis factor alpha, interleukin-2, lipopolysaccharide or phorbol myristic acetate, nor in human melanoma cell line SB-2 by uv irradiation, under conditions which induced the homologue CXC intercrine IL-8 expression. Furthermore, there was no induction of hIRH gene expression, but rather a suppression, upon serum or cytokine addition to serum-deprived fibroblast cell lines, to an in vitro mouse bone marrow preparation, and to monocytic cell line THP-1.
 ...
PMID:Reduced expression of the CXCR4 receptor mRNA in hepatocellular carcinoma and lack of inducibility of its ligand alpha-chemokine hIRH/SDF1alpha/PBSF in vitro. 1020 Mar 43

To examine the production of hepatocyte growth factor (HGF) by human endometrial stromal cells (ESC) in vitro, concentrations of HGF in the culture media of ESC were measured after the addition of various amounts of 12-O-tetradecanoylphorbol 13-acetate (TPA), forskolin, lipopolysaccharide (LPS), interleukin (IL)-1beta, IL-6, IL-8, tumor necrosis factor alpha (TNFalpha), interferon-gamma (IFNgamma), or ethynylestradiol-17alpha using an ELISA. The expression of HGF mRNA was also assayed by a reverse transcription-polymerase chain reaction. The concentration of HGF in the culture media of unstimulated ESC was below the detection level of the assay. TPA stimulated the secretion of HGF by ESC in a dose-dependent manner. TPA also induced the transcription of HGF mRNA by ESC. Forskolin, LPS, IL-1beta, IL-6, IL-8, TNFalpha, IFNgamma, or ethynylestradiol-17alpha did not alter HGF mRNA or protein levels. TPA-stimulated production of HGF was partially inhibited by the addition of 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine or sphingosine. These results suggest that a protein kinase C-dependent pathway may play an important role in the regulation of HGF production by ESC. HGF secreted by ESC may be involved in the regeneration of the endometrium during the normal menstrual cycle.
 ...
PMID:Expression of hepatocyte growth factor in cultured human endometrial stromal cells is induced through a protein kinase C-dependent pathway. 1020 81

PG490 (triptolide) is a diterpene triepoxide with potent immunosuppressive and antiinflammatory properties. PG490 inhibits interleukin(IL)-2 expression by normal human peripheral blood lymphocytes stimulated with phorbol 12-myristate 13-acetate (PMA) and antibody to CD3 (IC50 of 10 ng/ml), and with PMA and ionomycin (Iono, IC50 of 40 ng/ml). In Jurkat T-cells, PG490 inhibits PMA/Iono-stimulated IL-2 transcription. PG490 inhibits the induction of DNA binding activity at the purine-box/antigen receptor response element (ARRE)/nuclear factor of activated T-cells (NF-AT) target sequence but not at the NF-kappaB site. PG490 can completely inhibit transcriptional activation at the purine-box/ARRE/NF-AT and NF-kappaB target DNA sequences triggered by all stimuli examined (PMA, PMA/Iono, tumor necrosis factor-alpha). PG490 also inhibits PMA-stimulated activation of a chimeric transcription factor in which the C-terminal TA1 transactivation domain of NF-kappaB p65 is fused to the DNA binding domain of GAL4. In 16HBE human bronchial epithelial cells, IL-8 expression is regulated predominantly by NF-kappaB, and PG490 but not cyclosporin A can completely inhibit expression of IL-8. The mechanism of PG490 inhibition of cytokine gene expression differs from cyclosporin A and involves nuclear inhibition of transcriptional activation of NF-kappaB and the purine-box regulator operating at the ARRE/NF-AT site at a step after specific DNA binding.
 ...
PMID:Immunosuppressant PG490 (triptolide) inhibits T-cell interleukin-2 expression at the level of purine-box/nuclear factor of activated T-cells and NF-kappaB transcriptional activation. 1022 9

The increased number and early activation of cutaneous mast cells is a typical feature of psoriatic inflammation. Interferon-gamma (IFN-gamma) is believed to be one of the important mediators in the cytokine cascade of psoriasis. Human mast cells have been previously reported to release various cytokines upon stimulation including interleukin (IL) -4, IL-5, IL-6, IL-8, IL-13 and tumour necrosis factor-alpha. Here we report that human mast cells synthesize also IFN-gamma at mRNA and protein level and that the number of IFN-gamma producing mast cells is significantly increased in the psoriatic skin. IFN-gamma immunoreactivity in mast cells was demonstrated by staining non-lesional and lesional skin sections from 21 patients with psoriasis. Ten patients with atopic dermatitis (AD) and five healthy persons served as control groups. The percentage (mean +/- SD) of IFN-gamma + mast cells in lesional compared with non-lesional psoriatic skin was 67 +/- 18% vs. 44 +/- 17% (P < 0.0001, paired t-test), respectively, but only 9 +/- 6% vs. 10 +/- 7% in corresponding skin samples of AD. In the skin of healthy controls, only 12 +/- 12% of the mast cells were IFN-gamma +. Using immunoelectron microscopy, we confirmed the ultrastructural localization of IFN-gamma within the granules of mast cells in psoriatic skin. In addition, stimulation of a human mast cell line HMC-1 with phorbol myristate acetate (PMA) (100 nmol/L) for periods of 2-24 h induced expression of IFN-gamma mRNA, which peaked at 24 h. When HMC-1 cells were stimulated with PMA (100 nmol/L) for periods of 0-3 days, the cells released IFN-gamma protein, peaking on day 1. These results provide further evidence for the important role of mast cells in the pathogenesis of psoriasis.
 ...
PMID:Mast cells in psoriatic skin are strongly positive for interferon-gamma. 1023 11

Recent observations indicate that an antiinflammatory process may play a role in the metastatic cascade of renal cell carcinoma (RCC). Therefore, we compared the expression of cytokines from primary human RCC cultures, from established renal carcinoma cells and those from corresponding proximal renal tubulus cells. For this purpose the different cell types were treated with well defined and with bacterial substances such as the lipopolysaccharide, the staphylococcal enterotoxin B, a superantigen, or a combination of the calcium ionophore A23187 and phorbol 12-myristate-13-acetate. The resulting cell supernatants were analyzed for the proinflammatory cytokines (TNF-alpha, IL-6), the chemotactic active interleukin-8 as well as cytokines from T-helper type I (IL-2, IFN-gamma, IL-12) and type II (IL-4, IL-10). In parallel, the expression of cytokine-specific m-RNA was analyzed by multiplex-PCR. Our results clearly demonstrate that among the various cytokines analyzed a predominant release of TNF-alpha, IL-8 and IL-6 is obtained. The remainder cytokines were not detected independent whether molecular biology or cytokine release experiments were applied. Expression of the cytokines was dependent on the degree of malignancy. Among the applied stimuli, only the activation with calcium ionophore/phorbolester modulated cytokine expression and release. While TNF-alpha was induced from normal renal cells by up to 300% (2000 + 120 ng/10(5) cells) a pronounced suppression of TNF-alpha was observed in dependence on the malignancy of the cell line. In contrast, the cytokines IL-6 and IL-8 were significantly upregulated in malignant cells unlike in normal renal cells. These data suggest a differential role of the various cytokines derived from normal or tumor cells. Detailed studies will allow the understanding of the distinct roles of cytokines in renal carcinoma disease.
 ...
PMID:The differential expression of proinflammatory cytokines IL-6, IL-8 and TNF-alpha in renal cell carcinoma. 1036 36

Pregnancy can exert suppressive effects on chronic inflammatory conditions. We have previously demonstrated a depression in polymorphonuclear leukocyte (PMN) respiratory burst during pregnancy which could explain this amelioration. To elucidate the biochemical mechanism, we have examined PMN phospholipase A2 (PLA2) activity and its relationship to cellular and circulating fatty acids in pregnant women (30 to 34 weeks) and nonpregnant controls. PMN PLA2 activity was determined by arachidonic acid (AA) and leukotriene B4 (LTB4) release, respiratory burst activity was determined by lucigenin-enhanced chemiluminescence, and total serum and PMN fatty acid levels were determined by gas-liquid chromatography. AA release was significantly reduced for pregnancy PMNs in response to N-formyl-met-leu-phe (fMLP) under unprimed and tumor necrosis factor alpha (TNF-alpha)- or interleukin 8-primed conditions. Similarly, LTB4 liberation was significantly reduced in response to fMLP and phorbol myristate acetate in unprimed and TNF-alpha-primed pregnancy PMNs. All major fatty acid classes were altered in the pregnant state. Of these differences in PMNs, oleic acid and alpha-linolenic acid showed a significant increase (13 and 26%, respectively) and stearic acid and AA showed a significant decrease (8 and 30%, respectively). The stearic acid, oleic acid, and AA compositions of all cells analyzed correlated with their corresponding changes in serum fatty acid levels. Crossover serum incubations modified both fatty acid profiles and the PMN respiratory burst accordingly, while individual fatty acid incorporation studies highlighted the importance of polyunsaturated fatty acids for NADPH oxidase efficiency. These findings indicate that the attenuation of PMN function in pregnancy may originate from a reduction in the available pool of cellular fatty acids. Furthermore, this reduction arises as a direct result of a pregnancy-induced shift in circulating fatty acids from polyunsaturated to monounsaturated forms.
 ...
PMID:Significance of fatty acids in pregnancy-induced immunosuppression. 1039 68

Cytokine production by fibroblasts is not only important for immunological and inflammatory reactions in the epidermis and mucosa, but also for growth and differentiation of epithelial cells. To characterize the role of fibroblasts in the oropharyngeal mucosa, the expression of a panel of cytokines and cytokine receptors by fibroblasts isolated from normal human oropharyngeal mucosa was investigated by enzyme-linked immunosorbent assay (ELISA), reverse transcribed polymerase chain reaction (RT-PCR) and flow cytometry (FACS). Oropharyngeal fibroblasts produced the proinflammatory cytokines interleukin 1 alpha (IL-1 alpha), IL-6 and IL-8 without addition of phorbol-12-myristate-13-acetate (PMA) or biological response modifiers, suggesting an active involvement of these cells in host defence mechanisms. Keratinocyte growth factor (KGF), a growth factor for epithelial cells, and the angiogenetic fibroblast growth factors acidic and basic FGF (aFGF, bFGF) were also synthesized. Expression of receptors for IL-1, IL-4, IL-6, platelet-derived growth factor (PDGF) and epidermal growth factor (EGF) was found. These results indicate that oral fibroblasts are capable of producing a number of cytokines without the need for additional stimuli and emphasize their active regulatory role in the maintenance of the oral mucosa.
 ...
PMID:The role of fibroblasts from oropharyngeal mucosa in producing proinflammatory and mitogenic cytokines without prior stimulation. 1039 4

The migration of colonic epithelial cells (restitution) is an important event in the repair of mucosal injuries. Interleukin-8 (IL-8) is a physiological initiator of the chemotactic migration of leucocytes. This study aimed to determine whether IL-8 had a similar effect on migration in an in vitro model of wounded colonic epithelium. Cell migration over 24 h was assessed in circular wounds made in confluent monolayers of the human colon cancer cell line LIM1215. This migration was stimulated in a concentration-dependent manner by IL-8, with maximal effects of approx. 1.75-fold above basal migration. The motogenic effect of IL-8 was mediated independently of effects on cell proliferation. In contrast, it was partially dependent upon gene transcription and protein synthesis and involved the activation of pertussis-toxin-sensitive G-proteins. The short-chain fatty acids, acetate, propionate, butyrate and valerate, the activator of protein kinase C (phorbol-12-myristate-13-acetate) and tumour necrosis factor-alpha (TNF-alpha) all stimulated the secretion of IL-8. However, only the motogenic effect of TNF-alpha was dependent upon IL-8. In conclusion, IL-8 stimulated cell migration in an in vitro model of colonic epithelium, whereas the motogenic effect of at least one physiologically relevant factor was dependent upon an increase in its endogenous levels. If IL-8 stimulates colonic epithelial restitution in vivo, this would have ramifications for the control of repair processes following wounding of the colonic mucosa.
 ...
PMID:Interleukin-8 stimulates the migration of human colonic epithelial cells in vitro. 1046 65


<< Previous 1 2 3 4 5 6 7 8 9 10