Human ICAM-1 ELISA kit (4X96T)
- Known as:
- Human ICAM-1 Enzyme-linked immunosorbent assay test reagent (4X96T)
- Catalog number:
- lf-ek50070
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- Human ICAM-1 ELISA kit (4X96T)
Related genes to: Human ICAM-1 ELISA kit (4X96T)
- Gene:
- ICAM1 NIH gene
- Name:
- intercellular adhesion molecule 1
- Previous symbol:
- -
- Synonyms:
- BB2, CD54
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-04-24
- Date modifiied:
- 2016-01-15
Related products to: Human ICAM-1 ELISA kit (4X96T)
Related articles to: Human ICAM-1 ELISA kit (4X96T)
- Type II alveolar epithelial (ATII) cells play a central role in pulmonary homeostasis, epithelial repair, and innate antiviral defense. Polyinosinic: polycytidylic acid [Poly(I: C)], a synthetic analog of viral double-stranded RNA, induces a viral-like epithelial injury phenotype characterized by oxidative stress, mitochondrial dysfunction, inflammation, and inflammasome-associated responses. Small humanin-like peptide 2 (SHLP2), a mitochondrial-derived peptide, has been associated with cytoprotective and mitochondrial regulatory effects; however, its role in viral-like alveolar epithelial injury remains unclear. This study investigated the effects of SHLP2 on Poly(I: C)-induced cellular damage in human ATII cells. Human ATII cells were assigned to four groups: control, SHLP2 alone, Poly(I: C) alone, and subsequent SHLP2 treatment during continued Poly(I: C) exposure. Cell viability was assessed by MTT assay. Apoptosis was evaluated by Annexin V-FITC/PI flow cytometry and by measuring expression. Mitochondrial membrane potential and intracellular reactive oxygen species (ROS) production were analyzed. Oxidative stress-related markers, inflammatory mediators and antiviral response-associated markers, and inflammasome-associated molecules were evaluated by qPCR and ELISA. In silico protein-peptide docking was performed to predict possible interactions with SHLP2. Poly(I: C) reduced cell viability and promoted apoptosis, mitochondrial depolarization, and ROS accumulation in human ATII cells. These effects were accompanied by altered expression, increased and expression, changes in total NRF2 and KEAP1 protein levels, elevated inflammatory mediators and Poly(I: C)-induced antiviral response-associated markers, including TNF-α, IL-6, NF-κB, TICAM1, and IFN-β, and increases in NLRP3 inflammasome-associated markers, including NLRP3, cleaved caspase-1, IL-1β, and IL-18. SHLP2 alone did not exert cytotoxic effects. Notably, subsequent SHLP2 treatment during continued Poly(I: C) exposure attenuated apoptosis, mitochondrial depolarization, ROS accumulation, inflammatory mediator production, TICAM1 and IFN-β levels, and several inflammasome-associated markers and outputs. Docking analyses predicted possible interactions of SHLP2 with TICAM1 and KEAP1, providing hypothesis-generating in silico evidence for potential associations with inflammatory and redox-related proteins. SHLP2 treatment was associated with reduced mitochondrial depolarization, oxidative stress, and apoptosis, together with changes in inflammatory and antiviral response-associated markers and NLRP3 inflammasome-related outputs in Poly(I: C)-exposed human ATII cells. These findings identify SHLP2 as an early-stage candidate for further investigation in Poly(I: C)-induced viral-like alveolar epithelial injury. - Source: PubMed
Publication date: 2026/09/21
Ramazan Sara BetülTuran BedircanTurkkol AysegulÇalişkan Şerife GökçeOyur Merve EceAlici Muhammed HasanKolac Umut Kerem - Intron retention, a form of alternative RNA splicing, can occur as part of normal gene regulation or result from disruption of the splicing machinery. Retained introns can potentially form double-stranded RNA, activating innate immune sensors and inflammation. This mechanism has been implicated in cancer but has not been studied in neuropsychiatric diseases like alcohol use disorder. We systematically analysed transcriptome-wide intron retention events in brain tissue from 142 individuals (66 with alcohol use disorder and 76 controls), encompassing 320 region-specific samples from the superior frontal cortex, nucleus accumbens, central nucleus and basolateral amygdala. Analyses were adjusted for demographic, technical and biological covariates. Validation was performed in alcohol-preferring (P) rats using long-read sequencing. In complementary experiments, immunofluorescent staining was used to detect double-stranded RNA in rat brain tissue, while single-cell RNA-sequencing was performed to test activation of double-stranded RNA-sensing pathways in human brains. Brains from individuals with alcohol use disorder showed significantly higher total intron retention compared with controls, independent of age, with females showing greater increases than males. A total of 368 introns were positively associated with alcohol use disorder, and these introns were significantly longer and had weaker splice acceptor sites compared with non-associated introns. Genes harbouring these intron retention events were enriched in Purkinje neurons, visual cortex neurons and oligodendrocytes. Computational predictions indicated these long introns could form duplex RNA structures. Increased double-stranded RNA was confirmed experimentally in multiple brain regions of alcohol-consuming rats, where it co-localized primarily with neuronal nuclei and dendrites. In individuals with alcohol use disorder, we found that multiple pathways including double-stranded RNA responses, neuroinflammation, interferon and NF-κB signalling, adaptive immunity and apoptosis were activated. In addition, NeuN-positive neuronal counts significantly decreased in both the prefrontal and visual cortices. Furthermore, single-cell analysis demonstrated upregulation of TICAM1, the target of double-stranded RNA sensor TLR3, in oligodendrocytes, as well as widespread activation of downstream inflammatory pathways across glial and neuronal cell types. These findings provide the first evidence that chronic alcohol consumption promotes an overall increase of intron retention in the brain and is associated with the presence of double-stranded RNA. Furthermore, the double-stranded RNA may contribute to neuronal loss and brain pathology by activating a neuroinflammatory response. - Source: PubMed
Publication date: 2026/07/29
Li RudongReiter Jill LWyatt-Johnson Season KDong ChuanpengSmith Caine SGreen NickGao HongyuHauser Sheketha RKapoor ManavStevens JuliaMayfield R DayneGoate AlisonWang YueEdenberg Howard JBell Richard LSutherland Greg TrevorBrutkiewicz RandyLiu Yunlong - This study aimed to investigate the relationship between the molecular weight of carboxymethyl pachymaran (CMP) and its immunomodulatory activities, and to identify the molecular weight range responsible for activating the TLR4 pathways. Thirteen kinds of CMPs with different molecular weights ranging from 49 kDa to 655 kDa were obtained using enzymatic degradation. The structure of CMPs was characterized by FT-IR, NMR, XRD, TGA, and SEM. We found that the reduction in molecular weight modified the surface morphology of CMP, while the main structure remained unchanged. Our results indicated that CMP0 (655 kDa) failed to exert immunomodulatory effects by activating the TLR4/MyD88/NF-κB and TLR4/TRIF/IRF3 pathway. The CMPD12 (112 kDa) activated both TLR4/MyD88/NF-κB and TLR4/TRIF/IRF3 signaling pathways, promoted the secretion of NO, TNF-α, IL-6, IL-1β, and IFN-β in RAW264.7 cells, and induced M1 polarization, thereby exerting the optimal immunomodulatory activity. In contrast, CMPD60 (49 kDa) failed to activate the TLR4/MyD88/NF-κB pathway to induce the secrete of NO and cytokines in RAW264.7 cells, it only activated the TLR4/TRIF/IRF3 pathway to promote IFN-β secretion and M1 polarization in macrophages, exerting weak immunomodulatory activity. Our results revealed the molecular weight range responsible for the immunomodulatory activities of CMP, suggesting its potential application as an immunomodulating agent. - Source: PubMed
Publication date: 2026/07/18
Zhang LijiaHuang WenFeng XiMei ZhinanLiu Ying - High pathogenicity avian influenza (HPAI) poses a significant threat to poultry. Some chickens show resilience to HPAI, but the mechanisms involved are poorly understood. In this study, we aimed to identify the biological mechanisms associated with resilience to HPAIV infection in chickens. Chickens were inoculated with H7N1 HPAIV and classified as susceptible or resilient based on clinical signs, mortality, histopathological lesions, AIV antigen detection in tissues, and viral shedding. Blood transcriptomic analysis revealed that genes from resilient chickens are involved in the integrin-mediated signaling pathway (ITGA5, ITGA6, ITGB1), as well as in adaptive (BTK, TEC) and innate (TRIM13, LCK, TICAM1) immune pathways. Plasma proteomic profiling revealed that ARF4, EIF4A2, and HNRNPAB (proteins involved in fundamental cellular processes) were less abundant in resilient chickens compared to both controls and susceptible birds. Our results suggest that early modulation of these pathways is associated with resilience to HPAIV and likely reflects early viral control or reduced systemic dissemination rather than the absence of infection. - Source: PubMed
Publication date: 2026/08/06
Valdez-May María JPerlas AlbertNofrarías MiquelPina-Pedrero SoniaDabad MarcValle RosaPérez MartaMoreno-León AlejandroEsteve-Codina AnnaArgilaguet JordiBertran KateriMajó Natàlia - Pathogens, tissue damage, and cellular stress are detected by innate immune sensor molecules to drive inflammatory signaling and cell death. Mutations in the sensor NLRP1 are associated with inflammatory disease, but the regulation of this sensor is not well understood. Here, we find that LPS, a TLR4 ligand and canonical activator of innate immunity, inhibits NLRP1-mediated caspase activation, IL-18 release, and inflammatory cell death, PANoptosis. This inhibition requires TRIF but not MyD88, implicating TRIF-dependent TLR signaling. IRF3 is also required, suggesting an essential role for type I IFN signaling. Indeed, IFN-β production or treatment with exogenous IFN-α or IFN-β inhibits NLRP1-dependent PANoptosis in mouse bone marrow-derived macrophages and human macrophages and monocytes. Mechanistically, Nlrp1b/NLRP1 expression is significantly reduced in LPS- or type I IFN-treated cells. Overall, our study identifies a TLR4-TRIF-IRF3 signaling axis that induces type I IFNs to negatively regulate NLRP1 transcription, thereby blocking NLRP1-driven, caspase-1/caspase-8/RIPK3-dependent PANoptosis. These findings suggest type I IFNs as a potential therapeutic strategy for NLRP1-driven inflammatory diseases. - Source: PubMed
Publication date: 2026/07/29
Sharma Bhesh RajMummareddy HarisankeerthChadchan Sangappa BSarkar RomanEi Farran Chadi AKanneganti Thirumala-Devi