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0032 (0)16 41 44 07
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Česká republika Praha
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0032 (0)16 41 44 07
Recombinant Human Interleukin-8 (8-79) (IL8 /72)
(Cat. No.: C035)
Interleukin-8 (IL-8) belongs to the neutrophil-specific CXC family of chemokines. It is one of the initial cytokines released from a variety of cell types, including T cells, endothelial cells and fibroblasts, in response to an inflammatory stimulus and acts by recruiting neutrophils, T-cells and basophils to the site of inflammation. Elevated Interleukin-8 levels are associated with the onset of a variety of disease states.
Recombinant Human IL-8 (8-79) produced in E. coli is a single, non-glycosylated polypeptide chain containing 72 amino acids and having a molecular mass of 8452 Dalton.
Biological activity: rHuIL-8 /72 is fully biologically active when compared to standard. The ED50 as determined by its chemotaxis of hCXCR-2 transfected mouse BaF/3 cells is less then 2 ng/ml, corresponding to a Specific Activity of 5.0 x 105 IU/mg.
Purity: Greater than 95.0% as determined by:
(a) Analysis by RP-HPLC.
(b) Analysis by reducing and non-reducing SDS-PAGE Silver Stained gel.
Molecular weight: 9 KD+/-10% determined by reduced SDS-PAGE.
Amino-Acid Sequence: The sequence of the first five N-terminal amino acids was determined and was found to be Ser-Ala-Lys-Glu-Leu.
Endotoxin: Less than 0.1ng/µg (1 IEU/µg) determined by LAL test.
Lyophilized from a concentrated (1mg/ml) solution containing 20mM PBS pH-7.4 and 50mM sodium chloride.
Lyophilized rHuIL-8 /72 although stable at room temperature for 3 weeks, should be stored desiccated below -18°C. Upon reconstitution rHuIL-8 /72 should be stored at 4°C between 2-7 days and for future use below -18°C. For long-term storage it is recommended to add a carrier protein (0.1% HSA or BSA).
Please avoid freeze-thaw cycles.
It is recommended to reconstitute the lyophilized rHuIL-8 /72 in sterile 18MΩ-cm H2O not less than 100µg/ml, which can then be further diluted to other aqueous solutions.
1: Vet Immunol Immunopathol 2008
Modulation of ovine neutrophil function and apoptosis by standardized extracts of Echinacea angustifolia, Butea frondosa and Curcuma longa.
[Abstract] Impaired neutrophil function has been associated with increased infectious diseases in ruminants. Attachment of neutrophils to endothelium and superoxide production is critical features of their immune activity. Once the infection is cleared, programmed cell death ensures the rapid resolution of inflammation. To develop new natural therapeutics for ruminants, standard extracts of Echinacea angustifolia (Polinaceatrade mark), Butea frondosa and Curcuma longa (Curcuvettrade mark) were first evaluated on ovine neutrophil functions. Curcuvettrade mark strongly reduced PMA-stimulated adhesion and superoxide production. Polinaceatrade mark and B. frondosa extract also reduced these functions, but with less efficacy than Curcuvettrade mark. We analyzed the effect of
extracts on spontaneous apoptosis and gene expression in neutrophils aged in vitro for up to 22h. IL8 is critical for neutrophil recruitment and the immune response; Bcl2-related proteins, Bcl2A1 and Bax, are key regulators of neutrophil fate. Spontaneous apoptosis strongly increased in ovine neutrophils cultured for 22h (T22), accompanied by an upregulation of IL8 and a decreased Bcl2A1:Bax ratio. Curcuvettrade mark stimulated spontaneous apoptosis and inhibited IL8 and Bcl2A1 gene expression at T22, whereas Polinaceatrade mark and B. frondosa extract inhibited spontaneous apoptosis and stimulated IL8 expression at T22. These results suggest that Curcuvettrade mark has antiinflammatory activity, whereas Polinaceatrade mark and B. frondosa have an immunomodulatory action on sheep
2: Arterioscler Thromb Vasc Biol 2009 Jan;
Statins Control Oxidized LDL-Mediated Histone Modifications and Gene Expression in Cultured Human Endothelial Cells.
[Abstract] OBJECTIVE: Activation of the endothelium by oxidized low-density lipoprotein (oxLDL) has been implicated in the development of atherosclerosis. Histone modifications impact on the transcriptional activity state of genes. We tested the hypothesis that oxLDL-induced inflammatory gene expression is regulated by histone modifications and experienced the effect of statins on these alterations. METHODS AND RESULTS: OxLDL-related interleukin-8 (IL-8) and monocyte-chemoattractant protein-1 (MCP-1) secretion in endothelial cells was reduced by statins but enhanced by histone deacetylase inhibitors. OxLDL induced lectin-like oxidized LDL receptor-1 (LOX-1) and extracellular regulated kinases (ERK1/2)-dependent acetylation of histone H3 and H4 as well as phosphorylation
of histone H3, both globally and on the promoters of il8 and mcp1. Pretreatment of oxLDL-exposed cells with statins reduced the above mentioned histone modification, as well as recruitment of CREB binding protein (CBP) 300, NF-kappaB, and of RNA polymerase II but prevented loss of binding of histone deacetylase (HDAC)-1 and -2 at the il8 and mcp1 gene promoters. OxLDL reduced HDAC1 and 2 expression, and statins partly restored global HDAC-activity. Statin-related effects were reverted with mevalonate. In situ experiments indicated decreased expression of HDAC2 in endothelial cells in atherosclerotic plaques of human coronary arteries. CONCLUSIONS: Histone modifications seem to play an important role in atherosclerosis.
3: J Biol Chem 2008 Dec;
CXCL8/IL8 stimulates VEGF expression and the autocrine activation of VEGFR2 in endothelial cells by activating NFkappa B through the CBM (Carma3/Bcl10/Matl1) complex.
[Abstract] Vascular endothelial growth factor (VEGF) is a potent mitogen and permeability factor for endothelial cells that plays a central role in angiogenesis, vascular maintenance, inflammation and cancer. VEGF also mediates the homeostatic adaptation to hypoxic conditions by promoting an increase in vascular density to compensate for decreased oxygenation. This process is triggered by an oxygen-sensitive transcription factor, HIF1a, which becomes active in hypoxic tissues leading to the synthesis and secretion of VEGF. The role of HIF1a in other processes that involve angiogenesis such as in inflammation is less clear. Of interest, endothelial cells not only respond to but also store and secrete VEGF, which is required for the maintenance of the integrity of the
vascular system. How this intracellular pool of VEGF is regulated is still not understood. Here, we found that CXCL8/IL8, a potent pro-angiogenic and inflammatory chemokine, upregulates VEGF mRNA and protein levels in endothelial cells by acting on its cognate receptor, CXCR2, and that this results in the autocrine activation of VEGFR2. Surprisingly, this process does not involve HIF1a, but instead requires the activation of the transcription factor NFB. Furthermore, we identified the components of the CBM complex, Carma3, Bcl10 and Malt1 as key mediators of the CXCL8/IL8-induced NFB activation and VEGF upregulation. Together, these findings support the existence of a NFB-mediated pathway by which the pro-inflammatory chemokine CXCL8/IL8 controls the expression of VEGF in endothelial cells,
thereby promoting the activation of VEGF receptors in an autocrine fashion.
4: Mol Immunol 2008 Dec;
Broad early immune response of porcine epithelial jejunal IPI-2I cells to Entamoeba histolytica.
[Abstract] Amoebiasis caused by Entamoebahistolytica triggers an acute inflammatory response at early stages of intestinal infection. The patho-physiological study of intestinal amoebiasis requires the development of powerful animal models. Swine provide robust model for human diseases and they could be used to study intestinal amoebiasis. Here, we introduce an in vitro model of swine intestinal epithelial cell (IPI-2I) co-cultured with E. histolytica. Intestinal epithelial cells (IECs) have crucial roles in sensing pathogens and initiating innate immune response, which qualitatively influence adaptive immune response against them. The contact between the two cells induces marked macroscopic lesions of IEC monolayer and striking alteration of the IPI-2I cell phenotype
including blebbing, such as loss of attachment before to be phagocyte by the trophozoite. Increase in Lactate Dehydrogenase (LDH) levels in the culture supernatant of IECs was observed when ameba is present and could reflect the cellular cytotoxicity exerted by the parasite. Using quantitative real-time PCR, we identified the up-regulation of cytokines/chemokines implicated in neutrophil chemoattraction and inflammation, such as CCL2, CCL20, CXCL2, CXCL3, GM-CSF, IL1 alpha, IL6 and IL8, in response to the parasite that can further regulate the immunoregulatory functions of the immune cells of the host. The study points a cardinal role of these pro-inflammatory compounds as central mediators in the interaction IECs/ameba and suggests mechanisms by which they coordinate intestinal immune
response. This will focus future efforts on delineating the molecular and cellular mechanisms of other cell partners by the way of in vivo infection of swine.
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