Peptide 78
目录号 : GC63347
Peptide 78，一种趋化细胞因子，由 78 个氨基酸组成，是 IL-8 或 C-X-C 趋化因子超基因家族的蛋白成员。Peptide 78 诱导中性粒细胞 (PMN) 在类风湿性关节炎 (RA) 关节方面发挥重要作用。
Cas No.:132116-62-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Peptide 78, a chemotactic cytokine, a 78 amino acid protein member of the IL-8 or C-X-C chemokine supergene family. ENA-78 plays an important role in the elicitation of predominantly neutrophils (PMNs) into the joints of rheumatoid arthritis (RA)[1].
Peptide 78, a potent PMN chemotaxin, in the conditioned medium of human pulmonary epithelial cells (A549) stimulated with TNF-α (20 ng/mL) or IL-1β (10 ng/mL). Peptide 78 is an 8.3-kD protein with 78 amino acids containing 4 cysteines positioned identically to those of IL-8 and its homologues. Peptide 78 belongs to a supergene family that includes platelet factor-4, platelet basic protein, and its cleavage products (connective tissue activating peptide-III, β-thromboglobulin, and interferon-γ-inducible protein, macrophage inflammatory protein-2α, and macrophage inflammatory protein-2β)[1]. Peptide 78 shares several properties of PMN activation similar to either NAP-2 or LL-8. Peptide 78 stimulation of PMNs results in significant chemotactic activity, release of elastase from cytochalasin-B-pretreated cells, and the induction of free, cytosolic calcium release. Peptide 78 aids in the recruitment of PMNs into inflamed joints of RA. Peptide 78 represents one of the most abundant chemokines present in RA synovial fluid.Peptide 78 in rheumatoid arthritis synovial fluids is biologically active. Peptide 78 appears to account for almost half of the RA synovial fluid PMN chemotactic activity in vitro[1].
[1]. A E Koch, et al. Epithelial neutrophil activating peptide-78: a novel chemotactic cytokine for neutrophils in arthritis. J Clin Invest. 1994 Sep;94(3):1012-8.
| Cas No. | 132116-62-2 | SDF | |
| 分子式 | C62H107N23O21S | 分子量 | 1542.72 |
| 溶解度 | Water : 100 mg/mL (64.82 mM; Need ultrasonic) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.6482 mL | 3.241 mL | 6.4821 mL |
| 5 mM | 0.1296 mL | 0.6482 mL | 1.2964 mL |
| 10 mM | 0.0648 mL | 0.3241 mL | 0.6482 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Increased plasma levels of epithelial neutrophil-activating Peptide 78/CXCL5 during the remission of Neuromyelitis optica
BMC Neurol 2016 Jul 11;16:96.PMID:27401736DOI:10.1186/s12883-016-0622-3.
Background: In neuromyelitis optica (NMO), one of the underlying pathogenic mechanisms is the formation of antigen-antibody complexes which can trigger an inflammatory response by inducing the infiltration of neutrophils in lesions. Epithelial neutrophil-activating Peptide 78 (ENA 78), known as Chemokine (C-X-C motif) ligand 5 (CXCL5), belongs to the ELR-CXCL family. It recruits and activates neutrophils. The aim of this study was to evaluate ENA 78, IL-1β and TNF-α plasma levels in multiple sclerosis (MS) and neuromyelitis optica (NMO) patients. Methods: ENA 78, IL-1β and TNF-α plasma levels were detected in 20 healthy controls (HC), 25 MS and 25 NMO patients using MILLIPLEX® map Human High Sensitivity Cytokine/Chemokine Panels. Results: Plasma levels of ENA 78 were significantly higher in NMO patients than in HC (P < 0.001) and MS patients (P < 0.05). The NMO patients showed higher plasma levels of IL-1β compared with HC (P < 0.01). Further, increased plasma levels of TNF-α were found in the MS (P < 0.05) and NMO patients (P < 0.001). In addition, NMO patients had higher Expanded Disability Status Scale (EDSS) scores compared with MS patients (P < 0.05). EDSS scores were correlated with plasma levels of ENA 78 in NMO patients (P < 0.05). There were no significant correlations between EDSS scores and plasma levels of ENA 78 in MS patients (P > 0.05). Conclusions: The overproduction of pro-inflammatory cytokines such as IL-1β and TNF-α during the remission of NMO activates ENA 78, which in turn leads to neutrophil infiltration in lesions. ENA 78 plasma levels were correlated with EDSS scores in NMO patients. Elevated secretion of ENA 78 may be a critical step in neutrophil recruitment during the remission of NMO.
Implication of CXCL5 (epithelial neutrophil-activating Peptide 78) in the development of insulin resistance in patients with rheumatoid arthritis
Clin Exp Rheumatol 2019 May-Jun;37(3):373-379.PMID:30299246doi
Objectives: The chemokine molecule CXCL5 (C-X-C motif chemokine ligand 5, also known as epithelial neutrophil activating Peptide 78 -ENA78-) constitutes a link between obesity, inflammation and insulin resistance (IR) in the general population. CXCL5 has also been found to play a role in rheumatoid arthritis (RA) pathogenesis. Since chronic inflammation promotes IR and impairs pancreatic beta cell function in RA patients, we assessed the role of CXCL5 in the development of IR in RA. Methods: Cross-sectional study that encompassed 141 non-diabetic patients with RA. IR assessed by homeostatic model assessment (HOMA2), insulin and C-peptide serum levels and lipid profile, and CXCL5 serum levels were studied. Regression analysis was performed to evaluate how CXCL5 was related to IR, disease activity, and disease characteristics in RA patients. Results: HOMA2-IR indexes showed high values for both IR and beta cell production (%B), and low insulin sensitivity (%S) in patients with RA. C reactive protein (beta coef. 0.2 [95%CI -1.5-1.9], p=0.80) and disease activity through DAS28 (beta coef. 13 [95%CI -14-41], p=0.34) revealed no relation with CXCL5. Other disease characteristics, such as disease duration, serological status, or use of methotrexate or anti-TNF alpha therapies, were not associated with CXCL5 serum levels. While glucocorticoids were related to insulin, C-peptide serum levels, and HOMA2-IR and HOMA2-%B-C peptide, the use of prednisone was not associated with CXCL5 serum levels. Insulin and C peptide serum levels and IR indexes showed strong correlations among each other, but not with CXCL5 (insulin r2=-0.034, p=0.69; C peptide r2=-0.050, p=0.56). Conclusions: CXCL5 is not related to IR in RA patients. Therefore, the mechanisms leading to IR in patients with RA may be different from those in the general population.
Epithelial neutrophil-activating Peptide 78 concentrations are elevated in the peritoneal fluid of women with endometriosis
Fertil Steril 2003 Mar;79 Suppl 1:815-20.PMID:12620496DOI:10.1016/s0015-0282(02)04828-8.
Objective: To investigate the presence of epithelial neutrophil-activating Peptide 78 (ENA-78) in peritoneal fluid of women with and without endometriosis and to identify the cells that produce this inflammatory protein. Design: Case-control study. Setting: University hospital. Patient(s): Eighteen women with and 9 women without endometriosis. Main outcome measure(s): ENA-78 protein and mRNA levels were compared among women with and without endometriosis in samples of peritoneal fluid, samples of endometriotic lesions obtained by biopsy during laparoscopy, and peritoneal macrophages. Enzyme-linked immunosorbent assay, reverse transcription polymerase chain reaction, and in situ hybridization methods were used. Secretion of ENA-78 protein by interleukin-1beta-stimulated endometriotic stromal cells and in the media of lipopolysaccharide-stimulated peritoneal macrophages were compared to that in unstimulated cell cultures. Result(s): Peritoneal fluid concentrations of ENA-78 were significantly higher in affected women than in controls. Ectopic epithelial and stromal cells and peritoneal macrophages express ENA-78 messenger RNA. Interleukin-1beta stimulation of stromal cell cultures resulted in a 23-fold increase in ENA-78 concentration, and lipopolysaccharide stimulation of peritoneal macrophages increased concentrations by 8-fold. Conclusion(s): Levels of ENA-78 are elevated in the peritoneal fluid of women with endometriosis. Ectopic glandular cells, ectopic stromal cells, and peritoneal macrophages express this inflammatory chemokine. Epithelial neutrophil-activating Peptide 78 may play an important role in the pathogenesis of endometriosis.
Expression of epithelial neutrophil-activating Peptide 78 in cultured human endometrial stromal cells
Mol Hum Reprod 2001 May;7(5):453-8.PMID:11331668DOI:10.1093/molehr/7.5.453.
It has been demonstrated that human endometrial stromal cells (ESC) produce a variety of chemokines in vivo and in vitro. To evaluate the expression of epithelial neutrophil-activating Peptide 78 (ENA-78) in the endometrium, concentrations of ENA-78 in cyclic endometrial tissues were measured using enzyme-linked immunosorbent assay. The expression of ENA-78 was also detected in cyclic endometrium by immunohistochemistry. Endometrial tissues in the secretory phase contained higher amounts of ENA-78 protein than did those in the proliferative phase. Immunofluorescence staining revealed that ENA-78 protein was localized mainly in the stroma of endometrium. In addition, to evaluate the involvement of inflammatory mediators and ovarian steroid hormones in the production of ENA-78 by ESC was evaluated by in-vitro studies. Unstimulated ESC constitutively secreted ENA-78. Progesterone, lipopolysaccharide, tumour necrosis factor-alpha, and interleukin-1beta significantly stimulated the expression of ENA-78 by ESC. It is suggested that the production of ENA-78 by ESC is regulated by progesterone as well as by the inflammatory mediators. The modulation of ENA-78 concentration in the local environment by these mediators may contribute to the normal and pathological processes of human reproduction through regulation of leukocyte trafficking into the endometrium.
Citrullination of epithelial neutrophil-activating Peptide 78/CXCL5 results in conversion from a non-monocyte-recruiting chemokine to a monocyte-recruiting chemokine
Arthritis Rheumatol 2014 Oct;66(10):2716-27.PMID:24943990DOI:10.1002/art.38750.
Objective: To examine whether the citrullinated chemokines epithelial neutrophil-activating Peptide 78 (ENA-78)/CXCL5, macrophage inflammatory protein 1α/CCL3, and monocyte chemotactic protein 1/CCL2 are detected in the biologic fluid of patients with rheumatoid arthritis (RA), and if so, to determine the biologic activities of these chemokines. Methods: Recombinant human chemokines were citrullinated by peptidylarginine deiminase. Enzyme-linked immunosorbent assays were performed to measure the concentrations of citrullinated chemokines in sera from patients with rheumatoid arthritis (RA) and normal individuals and in synovial fluid from patients with RA, patients with osteoarthritis (OA), and patients with other inflammatory rheumatic diseases. The correlation between the citrullinated chemokine levels and clinical data was analyzed. Monocyte and neutrophil chemotaxis assays were performed, and native (noncitrullinated) or citrullinated ENA-78/CXCL5 was injected into mouse knees to evaluate the biologic activities of these chemokines. Results: The concentration of citrullinated ENA-78/CXCL5 was significantly higher in RA sera and SF than in normal sera and in SF from patients with other rheumatic diseases including OA. In RA SF, a strong correlation between the amount of citrullinated ENA-78/CXCL5 and the C-reactive protein level or the erythrocyte sedimentation rate was observed. Citrullinated ENA-78/CXCL5 induced monocyte chemotaxis via CXCR1 and CXCR2, while noncitrullinated ENA-78/CXCL5 did not. In a mouse model of inflammatory arthritis, citrullinated ENA-78/CXCL5 induced more severe inflammation and recruited more monocytes than did noncitrullinated ENA-78/CXCL5. Conclusion: Citrullinated ENA-78/CXCL5 is highly correlated with RA disease activity and, unlike noncitrullinated ENA-78/CXCL5, recruits monocytes. These results indicate that citrullinated ENA-78/CXCL5 may exert previously unrecognized inflammatory properties in RA by recruiting monocytes to inflamed joint tissue.