Cymax Human IL-8 ELISA Kit
- Known as:
- Cymax Human Interleukin-8 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- lf-ek0262
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- Cymax Human IL-8 ELISA Kit
Related genes to: Cymax Human IL-8 ELISA Kit
- Gene:
- CXCL8 NIH gene
- Name:
- C-X-C motif chemokine ligand 8
- Previous symbol:
- IL8
- Synonyms:
- SCYB8, LUCT, LECT, MDNCF, TSG-1, IL-8, NAP-1, 3-10C, MONAP, AMCF-I, LYNAP, NAF, b-ENAP, GCP-1, K60, GCP1, NAP1
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2016-10-05
- Gene:
- CXCR1 NIH gene
- Name:
- C-X-C motif chemokine receptor 1
- Previous symbol:
- CMKAR1, IL8RA
- Synonyms:
- CKR-1, CDw128a, CD181
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-09
- Date modifiied:
- 2016-03-14
- Gene:
- CXCR2 NIH gene
- Name:
- C-X-C motif chemokine receptor 2
- Previous symbol:
- IL8RB
- Synonyms:
- CMKAR2, CD182
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-19
- Date modifiied:
- 2016-03-14
- Gene:
- CXCR2P1 NIH gene
- Name:
- C-X-C motif chemokine receptor 2 pseudogene 1
- Previous symbol:
- IL8RBP, CXCR2P
- Synonyms:
- -
- Chromosome:
- 2q35
- Locus Type:
- pseudogene
- Date approved:
- 1992-11-27
- Date modifiied:
- 2016-03-14
Related products to: Cymax Human IL-8 ELISA Kit
Related articles to: Cymax Human IL-8 ELISA Kit
- Increasing evidence suggests that Porphyromonas gingivalis (Pg) is associated with oral squamous cell carcinoma (OSCC) development and progression. This study aimed to identify Pg-associated genes with prognostic relevance in OSCC through integrated bioinformatics analysis. - Source: PubMed
Publication date: 2026/08/27
Song QinZhang YouwenWu XiaodiPeng JiakuanZhao YihanZhang YanjunChen Xin - Primary mediastinal large B-cell lymphoma (PMBCL) predominantly affects female adolescents and young adults. It displays an immune-privileged phenotype and demonstrates the involvement of key cytokine signaling pathways, including increased expression of Thymus and activation-regulated chemokine (TARC/CCL17). Currently, there is a lack of established markers for stratification. We studied plasma concentrations of 24 cytokines at diagnosis in a large population-based pediatric cohort of 62 patients with PMBCL. Compared to a group of age-matched patients with other types of lymphoma in long-term remission and healthy individuals (n=26), we detected elevated concentrations of CCL4, CCL17, interleukin (IL)-6, CXCL8, CXCL9, CXCL10, and CXCL11. The median CCL17 level was 1695 pg/ml (IQR, 642-3142) in patients with PMBCL compared to 81 pg/ml (IQR, 41-190) in controls (p < 0.0001). Concentrations of CCL17, CXCL9, and CXCL10 significantly correlated with mediastinal tumor volume (MTV) and lactate dehydrogenase activity (LDH) but were not associated with event-free survival (EFS). Concentrations of IL-17F and IL-22 were inversely correlated with LDH and MTV. Elevated IL-6, IL-10, IL-17A, and IL-22 were significantly correlated with inferior EFS in a subgroup of 50 patients uniformly treated with dose-adjusted EPOCH with rituximab. Although based on a limited number of events, IL-6 showed the strongest association with outcome (hazard ratio of 6.8 (95%-CI, 1.5-30.9). In summary, pretreatment cytokine levels in patients with PMBCL reveal distinct patterns associated with tumor burden (CCL17, CXCL9, CXCL10) and outcome (IL-6, IL-10, IL-17A, IL-22). - Source: PubMed
Publication date: 2026/09/10
Nipper MalteDamm-Welk ChristineShepheard WillOschlies IlskeKlapper WolframBurkhardt BirgitWoessmann WilhelmKnörr Fabian - Keratinocytes coordinate re-epithelialization, barrier restoration, inflammatory control, and matrix remodeling during cutaneous repair. Although betanin has reported cytoprotective and antioxidant properties, its wound-relevant transcriptional program in keratinocytes remains incompletely defined. This study therefore asked whether betanin engages barrier, inflammatory, and remodeling-related keratinocyte programs under inflammatory conditions, and whether existing wound-healing databases can account for the resulting transcriptional pattern. Scratch closure was quantified by ImageJ measurement and by an independent rule-based automated image-analysis pipeline with first-order kinetic modeling; transcriptional responses in IFN-γ/TNF-α-stimulated HaCaT cells were interpreted through database-weighted evidence scoring and machine learning-based stress testing. Betanin (20 μg/mL) significantly reduced residual wound area at 24 h (p = 0.020) and 48 h (p = 0.035) by ImageJ quantification, and automated image analysis with kinetic modeling yielded an approximately 1.5-fold higher first-order closure rate constant relative to the vehicle-treated wounded control. Betanin partially restored FLG, reduced KRT14, and selectively attenuated inflammatory mediators including IL1B, ICAM1, CCL22, and CXCL8. Among remodeling-associated genes, TGFB1, COL1A1, and VEGFA were suppressed while COL3A1 was partially restored. NFE2L2 and HMOX1 were only modestly affected, indicating a dominant anti-inflammatory and barrier-modulating response rather than canonical antioxidant axis activation. Database-weighted evidence scoring stably prioritized FLG, COL3A1, COL1A1, and ICAM1, corroborated by betanin-specific experimental responses. Three architecturally distinct machine learning models showed no evidence that database-derived wound-healing features predict betanin-induced transcriptional responses, indicating that the selected prior-knowledge annotations were insufficient to account for the observed pattern in this 15-gene, single-context dataset. - Source: PubMed
Park Sun YoungKim Youjin - A high triglyceride/high-density lipoprotein cholesterol (TG/HDL-C) ratio is strongly associated with insulin resistance and atherosclerotic cardiovascular risk, but the cellular mechanisms linking this lipid imbalance to vascular injury remain incompletely defined. This study established a combined hyperglycemic/high TG/low HDL-C ratio-mimetic in vitro model using human coronary artery endothelial cells and THP-1-derived macrophages to investigate endothelial inflammation, glycocalyx disruption, monocyte recruitment, foam-cell formation, oxidative stress, and cholesterol efflux. High TG/low HDL-C ratio-mimetic stress significantly reduced endothelial viability, increased cytotoxicity, impaired transendothelial resistance, increased fluorescein isothiocyanate (FITC)-dextran permeability, and promoted syndecan-1 shedding. The lipid-stress condition induced endothelial inflammatory activation, with increased vascular cell adhesion molecule 1 (VCAM1), intercellular adhesion molecule 1 (ICAM1), E-selectin (SELE), C-C motif chemokine ligand 2 (CCL2), interleukin 6 (IL6), and C-X-C motif chemokine ligand 8 (CXCL8) expression, accompanied by enhanced THP-1 adhesion and transmigration. Glycocalyx and junctional injury were supported by increased heparanase (HPSE) expression and reduced syndecan-1 (SDC1), tight junction protein 1 (TJP1), cadherin 5 (CDH5), wheat germ agglutinin (WGA) staining, zonula occludens-1 (ZO-1) continuity, and vascular endothelial cadherin (VE-cadherin) integrity. Endothelial-conditioned lipid stress promoted macrophage foam-cell formation, increased CD36 scavenger receptor (CD36), oxidized low-density lipoprotein receptor 1 (OLR1), and peroxisome proliferator-activated receptor gamma (PPARG) expression, enhanced cholesterol accumulation, and suppressed ATP-binding cassette transporter A1 (ABCA1)-, ATP-binding cassette transporter G1 (ABCG1)-, scavenger receptor class B member 1 (SCARB1)-, and apolipoprotein E (APOE)-associated cholesterol efflux pathways. HDL rescue broadly attenuated endothelial inflammation, oxidative stress, barrier disruption, and macrophage foam-cell formation, whereas ApoA-I exerted protective effects across the selected endothelial and macrophage endpoints in which it was evaluated. CD36 inhibition reduced macrophage lipid accumulation, whereas heparanase inhibition preserved glycocalyx integrity. These findings identify the endothelial glycocalyx-nuclear factor kappa B (NF-κB)-CD36/ABCA1 axis as a mechanistic link between the high TG/low HDL-C ratio and diabetic atherosclerotic vascular dysfunction. - Source: PubMed
Publication date: 2026/09/10
Bi LechangZhao WenLu MingjingJiang NanWang GaofengHuang FeilaiLuo PengchaoWang Guofu - To assess STAT3 activation in peri-implantitis tissues and to evaluate the STAT3-associated response of oral epithelial cells (OECs) to peri-implantitis-associated bacteria. - Source: PubMed
Publication date: 2026/09/09
Arce MarionEspinoza-Arrue JoaquinSansores-España DanielMorales MatiasFarfan Mauricio JSanz MarianoAbusleme LoretoDutzan Nicolas