IL-8 Antibody, mAb, Mouse
- Known as:
- Interleukin-8 Antibody, mAb, Mouse
- Catalog number:
- a00044-500
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- IL-8 Antibody mAb Mouse
Related genes to: IL-8 Antibody, mAb, Mouse
- 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: IL-8 Antibody, mAb, Mouse
Related articles to: IL-8 Antibody, mAb, Mouse
- Degenerative lumbar spinal stenosis (LSS) is driven by fibrosis and hypertrophy of the ligamentum flavum (LF). Oxidative stress-an excess of reactive oxygen species (ROS) over antioxidant defenses-may underlie LF remodeling, but tissue-level evidence is limited. LF from patients with LSS (n = 180) and controls (n = 102) underwent transcriptomic microarray and microRNA (miRNA) profiling, reverse-transcription quantitative PCR (RT-qPCR), enzyme-linked immunosorbent assay (ELISA), and biochemical assays of thiobarbituric acid-reactive substances (TBARS), total glutathione (GSH), and glutathione peroxidase (GPx) activity. Protein-protein interaction (PPI) and functional enrichment analyses were performed. Among 14,130 oxidative-stress-related transcripts, 8,197 were differentially expressed (p < 0.05). Redox-sensitive inflammatory mediators were upregulated, including tumor necrosis factor (TNF), interleukin-1β (IL-1B), interleukin-6 (IL-6), and C-X-C motif chemokine ligand 8 (CXCL8), alongside mitogen-activated protein kinases (MAPK8/JNK1, MAPK14/p38α, MAPK1/ERK2) and superoxide dismutase 2 (SOD2) and peroxiredoxin-1 (PRDX1). Antioxidant defenses-catalase (CAT), superoxide dismutases SOD1/SOD3, glutathione peroxidase-1 (GPX1), and sirtuin-3 (SIRT3)-were downregulated. RT-qPCR confirmed these trends. ELISA demonstrated higher MAPK8 and IL-6 and lower SIRT3 and GPX1 in hypertrophic LF (all p < 0.05). Biochemically, LSS tissue showed increased TBARS and GPx activity and decreased GSH versus controls; oxidative imbalance intensified with greater pain and higher body mass index. Selected miRNAs (e.g., hsa-miR-3163→MAPK8, hsa-miR-4291→SIRT3) were reduced. PPI networks were highly enriched (p < 1 × 10⁻¹⁶). Notably, MAPK8, SIRT3, GPX1, and IL-6 dysregulation was independent of pain category. LF in LSS exhibits a persistent ROS-driven, MAPK-amplified inflammatory program with mitochondrial vulnerability (SIRT3 loss) and impaired peroxide detoxification (GPX1 decline). This oxidative signature likely sustains fibrosis and LF thickening and nominates MAPK8-SIRT3-GPX1-IL-6 as candidate biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/06/03
Strojny DamianSkóra KlaudiaKulpok TomaszWnuk ZygmuntNiedziałek WojciechSobański DawidStaszkiewicz RafałGrabarek Beniamin Oskar - The large yellow croaker (Larimichthys crocea) is one of the most economically important maricultured fish species in China. In recent years, the prevalence of large yellow croaker iridovirus (LYCIV) has caused significant economic losses to the large yellow croaker industry, highlighting the urgent need for research on disease-resistant breeding and opening new opportunities for disease control. Here, a genome-wide association study (GWAS) was conducted to identify loci associated with resistance to LYCIV, using a total of 420 fish (210 resistant and 210 susceptible) from a natural epidemic population in Xiapu, Ningde. Genotyping was performed using the 55K NingXin-III SNP array, yielding 44,780 high-quality SNPs. Two SNPs on chromosomes 14 and 24 were found to be significantly associated with disease resistance, explaining 5.20% and 4.06% of the phenotypic variance (PVE), respectively. The estimated heritability of host resistance to LYCIV was 0.33 ± 0.13. In addition, 28 candidate genes were identified as potentially responsible for this resistance. Based on their annotated functions, four candidate genes (jarid2b, cxcl8, kpna5, and stk26) were selected for further investigation. Temporal expression analysis following artificial infection demonstrated that these genes were upregulated by 10 d post-infection coinciding with the cessation of mortality, with cxcl8, kpna5, and stk26 showing significant induction, implicating their roles in host survival. Functional validation via overexpression in vitro revealed that jarid2b significantly suppressed LYCIV genome copies, whereas cxcl8, kpna5, and stk26 did not exhibit a significant effect on viral replication. Given the complexity of antiviral mechanisms in L. crocea, the specific modes of action of these candidate genes remain to be fully elucidated. These findings revealed the complex polygenic architecture underlying resistance to LYCIV in L. crocea, establishing a critical foundation for future in-depth studies on antiviral mechanisms and for enhancing host resistance through marker-assisted selection. - Source: PubMed
Publication date: 2026/06/02
Pan YingChi HongshuLin NengfengZeng JunjiaLiu XiaodongChen XiuxiaZheng ZaiyuJiang QiuhuanYu XunkaiGong Hui - During bacterial infections of the central nervous system (CNS), the glia-neutrophil axis can drive a vicious cycle that results in lethal neuroinflammation. However, it is becoming apparent that glia can also be a significant source of immunosuppressive factors following bacterial challenge, presumably to mitigate inflammatory CNS damage. Similarly, neutrophils are known to express anti-inflammatory mediators following activation but their ability to produce them in response to clinically important neurotropic bacteria is poorly understood. In the present study, we have characterized the responses of a differentiated human neutrophil cell line to Neisseria meningitidis challenge by RNA Tag-Seq analysis and show marked enrichment in the expression of genes associated with Toll-like receptor-mediated NF-κB and AP-1 signaling, and inflammatory gene products. Interestingly, we also describe their upregulated expression of EBI3, a molecule that can exert immunosuppressive effects outside of its role as a component of IL-27 and IL-35. We have confirmed that these neutrophils produce and secrete EBI3 following N. meningitidis challenge, and we have begun to assess the functional ramifications of such production with the demonstration that EBI3 can significantly reduce the production of CXCL8 by infected primary human astrocytes. These results raise the possibility that neutrophils recruited to the CNS during N. meningitidis infection produce EBI3, thereby limiting inflammatory glial responses to this neurotropic bacterium. - Source: PubMed
Publication date: 2026/06/01
Dunphy Andrew MKrueger Quinton AJohnson M BrittanyMarriott Ian - Molybdenum disulfide (MoS2), as an anticancer reagent, can absorb near-infrared (NIR) wavelengths in phototherapy. In the present study, the synergic effect of MoS2 (in nanostructure) and NIR radiation on human mesenchymal stem cells (hMSCs) was evaluated via protein-protein interaction (PPI) network analysis. Gene expression profiles of hMSCs were extracted from the Gene Expression Omnibus (GEO) database and analyzed via PPI network analysis. The validity of findings was assessed via the Kaplan-Meier Plotter. FN1, ACTA2, CCL2, CXCL8, FBN1, and LEP genes were selected as hub genes among 121 recognized differentially expressed genes (DEGs) as the targeted genes by the synergic effects of MoS2 and NIR radiation. Kaplan-Meier Plotter analysis demonstrated that FN1 suppression by MoS2 and NIR radiation can significantly increase the overall survival of patients with gastric cancer, lung cancer, ovarian cancer, and myeloma. In conclusion, findings indicate that the anticancer property of MoS2 is intensified in the condition of NIR radiation. Therefore, MoS2 is a suitable photosensitizer reagent in photodynamic therapy. - Source: PubMed
Publication date: 2026/02/14
Omidi Farzin AlirezaArjmand BabakAsri NastaranRazzaghi ZahraRazi FaridehBandarian FatemehRobati Reza MRezaei MitraVafaee RezaRahnamay Farnood Parnia - Vitiligo is a skin disease characterized by the loss of skin melanocytes, featuring the dual pathology of melanocyte damage due to oxidative stress and immune-mediated inflammation, which ultimately classifies it as an autoimmune condition. Sappanone A (SA), isolated from Caesalpinia sappan L., exhibits notable anti-oxidative stress and anti-inflammatory activity in various diseases. However, its potential effects and mechanisms in vitiligo remain uninvestigated. This study was designed to investigate the effects of SA on melanocytes and keratinocytes under oxidative stress and to evaluate its therapeutic potential in the monobenzone-induced vitiligo model. In vitro, SA protected PIG1 cells from HO-induced cytotoxicity and suppressed HMGB1 expression, nuclear export, and extracellular release. Furthermore, SA reduced HMGB1-induced overexpression of inflammatory cytokines in HaCaT cells, including CXCL8, CXCL9, CXCL10, CXCL11, and TNF-α. In vivo, SA administration alleviated monobenzone-induced depigmentation and CD8 T-cell infiltration in C57BL/6 mice. Transcriptomic analysis, protein-protein interaction network construction, and molecular docking revealed that Wnt5a may be a potential target of SA, and SA significantly reversed monobenzone-induced Wnt5a expression and activation of noncanonical Wnt signaling. Overall, SA effectively attenuated the HMGB1-mediated inflammatory response in keratinocytes. Furthermore, it exerted repigmentation effects in monobenzone-induced vitiligo mice via inhibiting the Wnt5a-mediated noncanonical Wnt signaling pathway. These results suggest that SA is a promising therapeutic candidate for vitiligo. - Source: PubMed
Publication date: 2026/06/02
Xu MingmingDing MeilinLi RuiZhang HejuanRen FeifeiLi HongyangZhang Wei