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)

Topical application of 1alpha,25-dihydroxyvitamin D3 (VD3) is thought to be beneficial in psoriasis because of its action in regulating keratinocyte proliferation and inflammation mediated by various cytokines. We assessed the effect of VD3 on the production levels of interferon (IFN)-alpha, interleukin (IL)-6, IL-8 and tumor necrosis factor (TNF)-alpha in mitogen-stimulated peripheral blood mononuclear cells (PBMC) of psoriatic patients. The results demonstrated that VD3 significantly inhibited IFN- , IL-6, and IL-8 levels produced by concanavalin A (Con A)-stimulated PBMC of psoriatic patients in a dose-dependent manner, and reduced mRNA expression for IFN- and IL-8. These findings suggest that in addition to the direct anti-proliferation effect on keratinocytes, VD3 may down-regulate the inflammatory cytokine production by infiltrating cells in psoriatic lesions.
 ...
PMID:Regulatory effects of 1alpha,25-dihydroxyvitamin D3 on inflammatory responses in psoriasis. 964 61

The observations that several types of viruses induced interleukin (IL)-8 production prompted us to investigate the interrelationship between IL-8 and cytomegalovirus (CMV) infection. CMV infection caused IL-8 production in a human monocytic cell line, THP-1, in dose- and time-dependent manners. Moreover, CMV induced IL-8 gene expression by concurrently activating transcription factors, NF-kappaB and AP-1. Furthermore, CMV infection of human fibroblast cell lines increased gene expression of a specific receptor for IL-8, CXCR1. IL-8 in turn enhanced CMV replication in a human embryonic fibroblast, MRC-5, in dose- and time-dependent manners. Augmented replication eventually culminated in the increased production of infectious CMV virions. Moreover, IL-8 can attenuate the antiviral activity of interferon (IFN), particularly that of alpha-type against picornaviruses such as encephalomyocarditis virus and poliovirus. The inhibitory effects were associated with reduced 2',5'-A oligoadenylate synthetase activity. These results would imply that CMV can induce IL-8, which can augment CMV replication directly and indirectly by counteracting antiviral activity of IFN.
 ...
PMID:Potential involvement of IL-8 in the pathogenesis of human cytomegalovirus infection. 966 76

Epidermal infiltration by neoplastic CD4+ T cells is a characteristic histologic feature of early stage mycosis fungoides, the most common type of cutaneous T cell lymphoma (CTCL). The mechanisms involved in epidermotropism are unknown. It has been suggested that the CXC chemokines IL-8 and interferon-gamma inducible protein 10 (IP-10) may play a role, but evidence that these chemokines are produced within the epidermis in epidermotropic CTCL is lacking. In this study skin biopsies from 17 CTCL patients, including 12 mycosis fungoides, four pleomorphic CTCL, and one CD8+ CTCL, were investigated for epidermal IL-8 and IP-10 mRNA expression by RNA in situ hybridization. In addition, the expression of monokine induced by gamma-interferon (Mig) mRNA, a CXC chemokine closely related to IP-10, was studied as well. The expression of IL-8 receptors A and B (CXCR1 and CXCR2, respectively) was investigated by immunohistochemistry. The results were correlated with the number and phenotype of epidermotropic T cells. Epidermal expression of IP-10 and Mig mRNA was detected in 10 of 11 and seven of 11 epidermotropic CTCL, respectively, but not in five nonepidermotropic CTCL biopsies or normal human skin. Epidermal IP-10 and Mig mRNA expression correlated with epidermal infiltration of CD4+ T cells, but not of CD8+ T cells. IL-8 mRNA was demonstrated in the epidermis of only two of 15 CTCL biopsies, and was associated, in both cases, with accumulation of neutrophils. Consistently, immunostaining of the (intraepidermal) T cells with antibodies against CXCR1 and CXCR2 was not observed. In conclusion, the results of this study indicate that IP-10, and to a lesser extent Mig, but not IL-8 is involved in the preferential infiltration of neoplastic CD4+ T cells in CTCL.
 ...
PMID:Epidermal interferon-gamma inducible protein-10 (IP-10) and monokine induced by gamma-interferon (Mig) but not IL-8 mRNA expression is associated with epidermotropism in cutaneous T cell lymphomas. 969 21

Nasal polyps are the most common mass lesion of the nasal cavity. Various pathogenetic mechanisms have been proposed. However, the cause is still largely unknown, and treatment methods have not been changed for several hundred years. In order to investigate the role of cytokines in the pathogenesis of nasal polyps, expression of cytokine messenger RNAs (mRNAs) in nasal polyps was investigated. We performed reverse transcriptase-polymerase chain reaction and Southern blot to examine gene expression of the cytokines interleukin (IL)-1 beta, IL-6, IL-8, transforming growth factor (TGF)-beta, IL-4, IL-5, and interferon (IFN)-gamma and compared the results with the gene expressions of these cytokines in normal nasal mucosa. Nasal polyp tissues were obtained from 14 patients undergoing polypectomy for nasal obstruction. Among them, 4 patients suffered from associated perennial allergic rhinitis. The mRNAs of IL-4 and IL-5 (Th2 cytokines) as well as IFN-gamma (Th1 cytokine) were expressed in all of the nasal polyps obtained from the 14 patients, irrespective of the presence or absence of allergy, while 2, 0, and 4 of 6 normal turbinate mucosae expressed IL-4, IL-5, and IFN-gamma mRNAs, respectively. The mRNAs of IL-1 beta, IL-6, IL-8, and TGF-beta were expressed in 6, 1, 2, and 3 of 6 normal turbinate mucosae, respectively, while the mRNAs of these cytokines were expressed in all of the 14 polyp tissues except IL-6 mRNA, which was expressed in 13 nasal polyp tissues. There were no differences in the mean density ratios of each cytokine band on Southern blot between polyp tissues with allergy and those without allergy. These results suggest that many cytokines are produced in nasal polyps, that they may play important roles in the pathogenesis of nasal polyps, and that allergy per se may not play a fundamental role in the pathogenesis of nasal polyps.
 ...
PMID:Cytokine gene expression in nasal polyps. 971 68

In a previous study, we demonstrated that the amount of interleukin (IL)-8 mRNA expressed by human gingival fibroblasts stimulated with lipopolysaccharide (LPS) from Prevotella intermedia ATCC 25611 is increased by pre-treatment with beta or gamma interferon (IFN-beta or -gamma). In the present study, we identified the regulatory effects of these IFNs on IL-8 mRNA expression and IL-8 production by human gingival fibroblasts. Priming with IFN-alpha (alpha), -beta, or -gamma upregulated the IL-8 mRNA expression in response to P. intermedia LPS, whereas co-stimulation with these IFNs reduced the amount of mRNA expressed by the cells. The regulation of IL-8 mRNA expression induced by recombinant human tumor necrosis factor-alpha (rHuTNF-alpha) or rHuIL-1alpha was similar to that induced by LPS. The IL-8 mRNA expression in response to P. intermedia LPS was enhanced by IFN-gamma independently of de novo protein synthesis, and was regulated, at least in part, at the transcriptional level. The IL-8 mRNA accumulation in response to P. intermedia LPS was inhibited by tosylphenyl-alanyl chloromethyl-ketone, an inhibitor of NF-kappaB activation, although the NF-kappaB activation itself was not altered by IFN-gamma. These findings suggest that IFNs might be capable of both enhancing and inhibiting inflammatory responses in periodontal tissues through the dual regulation of IL-8 production by gingival fibroblasts in response to bacterial components and cytokines.
 ...
PMID:Dual regulatory effects of interferon-alpha, -beta, and -gamma on interleukin-8 gene expression by human gingival fibroblasts in culture upon stimulation with lipopolysaccharide from Prevotella intermedia, interleukin-1alpha, or tumor necrosis factor-alpha. 971 33

Inhibitors of p38 mitogen-activated protein kinase (p38) have been reported to block tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) production in monocytes at the level of mRNA translation. Yet, several studies document that p38 can phosphorylate and activate specific transcription factors. Thus, to understand better the role of p38 during monocyte activation, we sought to determine the extent to which p38 is required for lipopolysaccharide (LPS)-induced gene expression. For this, differential mRNA display was used to identify LPS-induced genes whose expression was blocked by SB202190, a specific inhibitor of p38. A partial screen identified 10 genes in monoyctes induced 4- to 74-fold by LPS. Of these, genes encoding interferon-induced gene 15, neuroleukin, radiation-inducible immediate-early gene-1, A20, IL-1beta, and superoxide dismutase were suppressed >50% by SB202190. LPS-induced gene activation was not blocked by cycloheximide, indicating that synthesis of intermediate proteins was not required. SB202190 blocked gene induction by 50% when present between 41 and 123 nM, consistent with the potency of this compound as a p38 inhibitor. Furthermore, the ability of SB202190 to block gene activation was stimulus-dependent. LPS and interferon-alpha (IFN-alpha) both up-regulated neuroleukin mRNA, but only LPS-induced neuroleukin mRNA was suppressed by SB202190. In contrast, TNF-alpha and LPS both induced IL-8 mRNA, and induction by either TNF-alpha or LPS was blocked by SB202190. These data were consistent with the ability of LPS and TNF-alpha, but not IFN-alpha, to activate p38 in monocytes. The results provide pharmacological evidence that p38 may be a key mediator of inducible gene expression in monocytes, but its role is stimulus and gene specific.
 ...
PMID:SB202190, a selective inhibitor of p38 mitogen-activated protein kinase, is a powerful regulator of LPS-induced mRNAs in monocytes. 973 69

The capacity of T cells to produce cytokines was investigated using T-cell clones (TCCs) established from infiltrating cells in the aqueous humor (AH) or peripheral blood mononuclear cells (PBMC) of patients with Vogt-Koyanagi-Harada (VKH) disease or sarcoidosis. The cytokines produced and tested in the study were interleukin (IL)-1alpha, IL-6, IL-8, interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, and granulocyte monocyte colony stimulating factor (GM-CSF). All TCCs (n = 9) from AH of VKH patients spontaneously produced significantly larger amounts of IL-6, IL-8, and IFN-gamma than TCCs from healthy donor PBMC. All TCCs (n = 9) from AH of the sarcoidosis patient spontaneously produced significantly larger amounts of IL-1alpha, IL-6, and IL-8 than TCCs from healthy donor PBMC. In addition, the effects of antiinflammatory drugs on the cytokine production by the TCCs were investigated. Hydrocortisone significantly suppressed the production of IL-6, IL-8, and GM-CSF by TCCs from AH of VKH patients. Tacrolimus also significantly suppressed the production of IL-8 and GM-CSF by the TCCs. FTY720, an experimental drug, suppressed only GM-CSF production by TCCs from AH of VKH patients. Diclofenac failed to suppress the production of any cytokines by any TCCs. All tested drugs did not suppress the production of cytokines by TCCs from the sarcoidosis patient. These results thus suggest that cytokines produced by T cells infiltrating in the eye may play an important role in the pathogenesis of uveitis.
 ...
PMID:Cytokine production by T cells infiltrating in the eye of uveitis patients. 974 65

Cytokines are suspected to play a crucial role in the pathogenesis of Helicobacter pylori-associated gastric diseases. Hence, considerable attention has been paid to the actions of cytokines on gastric cells. We examined the effects of cytokines on mucus secretion by gastric epithelial cells, without or with H. pylori components. Mucus secretion by cultured gastric epithelial cells was assessed as secretion of [3H]glucosamine-prelabeled high-molecular-weight glycoproteins. Interleukin (IL)-1beta and IL-6 significantly stimulated mucus secretion, but other cytokines such as IL-7, IL-8, IL-10, interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha had no effect. H. pylori lysate caused a decrease in both basal and stimulated secretion of mucus. In addition, IFN-gamma significantly potentiated the lysate-induced reduction of basal and stimulated secretion. Cell viability was not affected by any of treatments. These results indicate that IL-1beta and IL-6 stimulate mucus secretion, while IFN-gamma potentiates H. pylori-decreased secretion by gastric epithelial cells.
 ...
PMID:Effects of cytokines, without and with Helicobacter pylori components, on mucus secretion by cultured gastric epithelial cells. 979 Apr 69

Nitric oxide produced by inducible nitric oxide synthase (iNOS) has been claimed to be involved in gastritis; however, its characteristics are largely unknown. We assessed (1) iNOS expression in the human gastric mucosa in chronic gastritis and (2) the cytokines associated with iNOS expression. Gastric biopsy specimens were obtained from patients with chronic gastritis. Total RNA was isolated and reverse transcription-polymerase chain reaction (PCR) was performed semiquantitatively using specific primer sets for iNOS, interleukin (IL)-1beta, IL-8, IL-6, interferon-y, tumor necrosis factor-alpha (TNF-alpha), TNF receptors, IL-6 receptors, and sucrase, respectively. Helicobacter pylori infection was examined by the PCR assay. Reverse transcription-PCR analysis showed that expression of iNOS was detected in 10 of 23 samples. Expression of iNOS mRNA was closely correlated with expression of TNF-alpha and was observed frequently in subjects with intestinal metaplasia. The Helicobacter pylori gene was detected by PCR assay in all iNOS-positive cases. These results indicate that iNOS is predominantly expressed in the gastric mucosa with intestinal metaplasia and H. pylori infection. TNF-alpha is thought to be an important cytokine associated with iNOS expression.
 ...
PMID:Enhanced expression of inducible nitric oxide synthase in chronic gastritis with intestinal metaplasia. 980 53

The present study was to determine whether the administration of a single dose of interferon-alpha2B (IFN-alpha2B) to healthy humans affects endogenous (or basal level) or inducible cytokines in a whole blood, ex vivo culture. Twenty-four healthy volunteers received an s.c. injection of IFN-alpha2b (3 x 10(6)U), and 4 volunteers received the vehicle as placebo. The study was blinded. Blood was drawn before and 3, 6, 12, and 24 h after the injection and incubated in the presence or absence of lipopolysaccharide (LPS) or interleukin-1beta (IL-1beta). After 24 hs, the plasma was assayed for tumor necrosis factor-alpha (TNF-alpha), IFN-gamma, IL-1beta, IL-1 receptor antagonist (IL-1Ra), and IL-8. Treatment with IFN-alpha2b was associated with a 4.8-fold increase in the endogenous production of IL-1Ra in cultured blood sustained over 24 hs. In contrast, no change in endogenous IL-1Ra production was detected in the controls. A significant suppression (75%, p < 0.001) of IL-1beta-induced IL-8 production 3 and 6 h after IFN-alpha2b compared with control subjects was observed. These effects were also observed when IFN-alpha2b was added directly to whole blood cultures in vitro. In contrast to IL-1 stimulation, LPS stimulation of blood from IFN-alpha2b-treated subjects resulted in enhanced IL-1beta and TNF-alpha production. These results suggest that a single dose of IFN-alpha2b induces an anti-inflammatory state for endogenous stimuli but a proinflammatory state for exogenous endotoxin.
 ...
PMID:Spontaneous and inducible cytokine responses in healthy humans receiving a single dose of IFN-alpha2b: increased production of interleukin-1 receptor antagonist and suppression of IL-1-induced IL-8. 980 26


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