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)

Since the discovery of cytokines as key mediators in inflammation, targeting the cytokine network has represented a promising therapeutic approach. Psoriasis and atopic dermatitis, as T cell-mediated diseases with a strong cytokine component and a high unmet medical need, have moved into the focus of experimental therapies. Whereas pro-inflammatory cytokines such as tumor necrosis factor (TNF)-alpha are overexpressed in both diseases, a type 1 cytokine pattern predominates in psoriasis and a type 2 cytokine pattern is of pathophysiological importance at least in the initial stages of atopic dermatitis. Strategies for intervention into the cytokine network have included antagonism of pro-inflammatory cytokines (e.g. TNFalpha, interleukin [IL]-1, IL-8, IL-12, IL-18, IL-23) with neutralizing antibodies and soluble receptors, application of recombinant cytokines (e.g. IL-4, IL-10, IL-11, interferon [IFN]-gamma) to shift the cytokine balance, and administration of small molecules to modulate cytokine expression or signaling. Results from the clinic have led to novel therapeutic options as well as a better understanding of the pathophysiology of inflammatory skin diseases. This review highlights the various therapeutic strategies, results from the clinic (that are in some cases preliminary), and insights that can be drawn from the more advanced clinical studies and the use of approved cytokine-directed therapies.
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PMID:Cytokine and anti-cytokine therapies for psoriasis and atopic dermatitis. 1662 67

Since previous results showed that interleukin 8 (IL-8) was induced in rainbow trout (Oncorhynchus mykiss) in response to viral hemorrhagic septicemia virus (VHSV) infection, we have cloned IL-8 in an expression vector (pIL8+) and studied its possible adjuvant effect on the early response to a VHSV immunization model, focusing on the early response of several cytokines induced by a vector coding for the glycoprotein of VHSV (pMCV1.4-G) in the spleen and head kidney. First, we demonstrated that the pIL8+ successfully transcribed IL-8, by induction of IL-8 transcription in the muscle and blood, and by a massive infiltration of neutrophils at the muscle inoculation site. We have studied the effect of pIL8+ co-administration on the expression of two pro-inflammatory cytokines, such as IL-1beta and tumour necrosis factor alpha (TNF-alpha); cytokines that have mainly an inhibitory role, IL-11 and transforming growth factor beta (TGF-beta); and a Th1 type cytokine, IL-18. We demonstrated that the co-administration of pIL8+ with pMCV1.4-G modulates the cytokine response that is induced, mainly by having its effect increasing pro-inflammatory cytokines (IL-1beta and TNF-alpha1), with a greater impact on the spleen, and to a lesser extent in the head kidney. All these data suggest that IL-8 is able to modulate the early cytokine immune response that is produced in response to a DNA vaccine, and therefore, might be a potential immune adjuvant in fish viral vaccination. More work should be done to determine if this modulation has a beneficial effect on protection as seen in other mammal viral models.
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PMID:Co-injection of interleukin 8 with the glycoprotein gene from viral haemorrhagic septicemia virus (VHSV) modulates the cytokine response in rainbow trout (Oncorhynchus mykiss). 1672 33

Cytokines are peptides that are produced by virtually every nucleated cell type in the body, possess overlapping biological activities, exert different effects at different concentrations, can either synergize or antagonize the effects of other cytokines, are regulated in a complex manner, and function via cytokine cascades. Hyperoxia-induced acute lung injury (HALI) is characterized by an influx of inflammatory cells, increased pulmonary permeability, and endothelial and epithelial cell injury/death. Some of these effects are orchestrated by cytokines. There are significant differences in the response of the developing versus the adult lung to hyperoxia. We review here cytokines (and select growth factors) that are involved in tolerance toward HALI in animal models. Increased cytokine expression and release have a cascade effect in HALI. IL-1 precedes the increase in IL-6 and CINC-1/IL-8 and this seems to predate the influx of inflammatory cells. Inflammatory cells in the alveolar space amplify the lung damage. Other cytokines that are primarily involved in this inflammatory response include IFN-gamma, MCP-1, and MIP-2. Certain cytokines (and growth factors) seem to ameliorate HALI by affecting cell death pathways. These include GM-CSF, KGF, IL-11, IL-13, and VEGF. There are significant differences in the type and temporal sequence of cytokine expression and release in the adult and newborn lung in response to hyperoxia. The newborn lung is greatly resistant to hyperoxia compared to the adult. The delayed increase in lung IL-1 and IL-6 in the newborn could induce protective factors that would help in the resolution of hyperoxia-induced injury. Designing a therapeutic approach to counteract oxygen toxicity in the adult and immature lung first needs understanding of the unique responses in each scenario.
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PMID:Cytokines in tolerance to hyperoxia-induced injury in the developing and adult lung. 1678 48

In recent decades many advances have occurred in the understanding of the role of cytokines in breast cancer. New signalling pathways of interleukin (IL)-1 family, IL-6, IL-11, IL-18, interferons (IFNs) and interferon regulatory factors 1 (IRF-1) and 2 (IRF-2) have been found within tumour microenvironments and in metastatic sites. Some cytokines (IL-1, IL-6, IL-11, TGFbeta) stimulate while others (IL-12, IL-18, IFNs) inhibit breast cancer proliferation and/or invasion. Similarly, high circulating levels of some cytokines seem to be favourable (soluble IL-2R) while others are unfavourable (IL-1beta, IL-6, IL-8, IL-10, IL-18, gp130) prognostic indicators. So far IL-2, IFNalpha, IFNbeta and occasionally IFNgamma, IL-6, IL-12 have been the cytokines used for anti tumour treatment of advanced breast cancer either to induce or increase hormone sensitivity and/or to stimulate cellular immunity. Disappointing results occurred in most trials; however, two long-term pilot studies suggest that IL-2 and IFNbeta, when used appropriately can have a positive effect on clinical benefit and overall survival of patients with minimal residual disease after chemotherapy or with disseminated disease controlled by conventional endocrine therapy.
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PMID:Cytokines in breast cancer. 1693 Nov 7

Alternations in airway wall architecture, particularly increased smooth muscle mass are associated with pathogenesis of asthma. Muscle fiber hyperplasia and hypertrophy is a major contributor to the increase in smooth muscle mass. Airway smooth muscle was traditionally considered to have only contractile and proliferative functions and has little attention with regard to its ability to express and release inflammatory mediators. Airway smooth muscle cells have been shown to release cytokines such as: GM-CSF, IL-11, IL-6, IL-1, IL-5, IL-8, PGs and NO. Airway remodeling has been shown to respond to some degree anti-inflammatory therapy. Several study results indicate that steroid can positively influence progressive airflow limitation. Combined use of a beta2-agonist and steroid can reduced the remodeling progression.
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PMID:[Alternations of bronchial smooth muscle and effect of therapy on remodeling in asthma]. 1700 82

Papillomatous digital dermatitis (PDD) is a polymicrobial infection in soft tissue adjacent to the hoof and is the leading cause of lameness in dairy cattle. Treponema phagedenis-like (TPL) spirochetes are a constant feature of PDD lesions and are localized deep in infected tissue. Host-cell response mechanisms to TPL spirochetes are poorly understood. To assess how bovine macrophages respond to cellular constituents of TPL spirochetes, changes in transcription were analyzed using serial analysis of gene expression (SAGE) and real time RT-PCR. This analysis revealed that some proinflammatory cytokines (e.g. GCP-2 and IL-8) are induced in treated macrophages, while receptors and their accessory proteins for IL-1, IL-6 and IL-11 are either down regulated or unchanged. Two genes encoding proteins having negative effects on NFkappaB, IkappaB and SIVA-1, are significantly induced in stimulated cells. Several genes associated with the cytoskeleton and antigen presentation are down regulated after exposure to sonicated TPL spirochetes, as are genes associated with wound repair. Combined, these data suggest that the innate immune and wound repair functions of bovine macrophages exposed to TPL cellular constituents are impaired thereby enabling bacteria to resist clearance and induce lesion formation. Use of this in vitro bovine macrophage model should be useful in elucidating host-spirochete interactions and facilitate identification of potential virulence traits.
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PMID:Papillomatous digital dermatitis spirochetes suppress the bovine macrophage innate immune response. 1762 59

Long term loosening of hip prostheses remains an important problem in orthopedics. Although various loosening mechanisms have been proposed, the exact process is still unclear. Particle disease and the pressure theory are widely known and generally accepted hypotheses to explain long term implant failure. Each proposed mechanism recognizes a local inflammatory response in which macrophages represent the main cell-type and several proinflammatory and antiinflammatory cytokines (IL-1beta, IL-6, TNFalpha, IL-10, TGFbeta), chemokines (IL-8/CXCL8, MCP-1/CCL2, RANTES/CCL5, MIP-1alpha/CCL3) and other mediators (GM-CSF, M-CSF, MMP-1, PDGF-alpha, PGE(2), IL-11) are identified. The cytokines have different functions and some are capable of stimulating bone resorption in various ways; either directly or indirectly. Even though the implant loosening is thought to be "aseptic", several studies suggested a possible role for bacteria and a bacterial biofilm in implant failure. Biofilm-derived bacteria and bacterial products might have an underestimated and potential role in the loosening process. In this article we will discuss the possible role of a bacterial biofilm and the importance of the local surrounding environment in "aseptic" loosening of hip prostheses.
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PMID:The local inflammatory environment and microorganisms in "aseptic" loosening of hip prostheses. 1809

The impressive correlation between cardiovascular disease and alterations in glucose metabolism has raised the likelihood that atherosclerosis and type 2 diabetes may share common antecedents. Inflammation is emerging as a conceivable etiologic mechanism for both. Interleukins are regulatory proteins with ability to accelerate or inhibit inflammatory processes, and matrixins are prepro enzymes responsible for the timely breakdown of extracellular matrix. Interleukins (ILs) are classified based on their role in diabetes and atherosclerosis, hypothesizing that each interleukin acts on both diseases in the same direction - regardless if harmful, favorable or neutral. They are clustered into three groups: noxious (the 'bad', 8 members), comprising IL-1, IL-2, IL-6, IL-7, IL-8, IL-15, IL-17 and IL-18; protective (the 'good', 5 members), comprising IL-4, IL-10, IL-11, IL-12 and IL-13; and 'aloof' , comprising IL-5, IL-9, IL-14, IL-16 and IL-19 through IL-29 (15 members). Each group presented converging effects on both diseases. IL-3 was reluctant to clustering and IL-30 through 33 were not included due to the scarce available data. It may be seen that (1) favorable effects of a given interleukin on either diabetes or atherosclerosis predicts similar effects on the other; (2) equally, harmful interleukin effects on one disease can be extrapolated to the other, and (3) absence of influence of a given interleukin on one of these diseases forecasts lack of effects on the other. Matrixins seem to present a similar pathophysiological pattern. These facts further support the unifying etiologic theory of diabetes and heart disease, emphasizing the importance of a cardiovascular diabetologic approach to these cytokines for future research. A pharmacologic simultaneous targeting of interleukins and matrixins might provide an effective means to concurrently control both atherosclerosis and diabetes.
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PMID:Biomarkers in cardiovascular diabetology: interleukins and matrixins. 1823 Sep 55

The expression of cytokines and cytokine receptors was investigated in enriched populations of human fetal Schwann cells by reverse transcribed-PCR and enzyme-linked immunosorbent assay. Human fetal Schwann cells constitutively expressed mRNA of IL-1beta, IL-6, IL-8, IL-11, IL-12, IL-15 and TGF-beta, and also cytokine receptors for IL-1, IL-4, IL-6, IL-8, IL-13, tissue necrosis factor and gp130. The expression of IL-1beta, IL-6 and IL-15 was upregulated following treatment with IL-1beta or TGF-beta. The protein levels of IL-6 were increased with IL-1beta treatment, but were decreased with IFN-gamma treatment. Human Schwann cells may respond to cytokine signals in the nerve injury sites and modify the pathological conditions by secreting cytokines. The secreted cytokines may play a role in leukocyte recruitment and exacerbation of axonal injury process.
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PMID:Expression of cytokines and cytokine receptors in human Schwann cells. 1828 88

Psoriasis is a common skin disease involving 1-4% of human population worldwide, of strong genetic background. The following cytokines are directly involved in psoriasis: TNF, IL-1, IL-2, IL-6, IL-7, IL-8, IL-15, IL-18, IL-19, IL-20, IL-23 whereas IL-4, IL-10, IL-12 as well as IL-11, IL-17 and IFN-gamma are rather indirectly engaged. This work is a review of some genetic factors and structure of selected cytokines and receptors and their genes location.
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PMID:Genes and structure of selected cytokines involved in pathogenesis of psoriasis. 1829 59


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