MIP_3a
- Known as:
- MIP_3a
- Catalog number:
- ANT-212
- Product Quantity:
- 500µg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- MIP_3a
Related products to: MIP_3a
Related articles to: MIP_3a
- Vancomycin (VAN) is widely used in sepsis but may exacerbate sepsis-associated acute kidney injury (SA-AKI). The mechanisms by which VAN aggravates renal injury in the septic context remain unclear, and early functional changes are difficult to detect using conventional biomarkers. - Source: PubMed
Publication date: 2026/05/12
Liu YuxiLiu LinqiongLi HongxuYuan MengyaoShen LifengXin YuLiu YanqiShi ZeyuZhou QinyuanGao YanWang ChangsongYu Kaijiang - Psoriasis (PSO) is a chronic immune-mediated inflammatory skin disease characterized by keratinocyte hyperproliferation and dysregulated activation of the IL-23/IL-17 axis, leading to persistent cutaneous inflammation and substantial disease burden. Comprehensive profiling of circulating inflammatory proteins provides important insights into the systemic immune alterations associated with PSO and its treatment. However, the longitudinal plasma proteomic changes induced by IL-17A blockade remain incompletely characterized. - Source: PubMed
Publication date: 2026/04/24
Zhang HongyangYang RuiMa YuYang JiahuiYang BinyanDong LingdiYu Nan - Alyssin is an isothiocyanate found in cruciferous plants, and it has been reported to have physiologically active effects. However, there have been no attempts to use alyssin for the treatment of periodontitis, and there are no reports investigating the effects of alyssin on periodontal tissue component cells. In this study, experiments were conducted to determine whether alyssin has an anti-inflammatory effect on human periodontal ligament cells. - Source: PubMed
Publication date: 2026/05/11
Hosokawa IkukoHosokawa YoshitakaOkamoto RisaOzaki KazumiHosaka Keiichi - Platelet-rich fibrin (PRF) is extensively utilized to enhance localized tissue healing, a process that critically depends on the transient polarization of macrophages toward a pro-inflammatory phenotype. Given that PRF, like other blood clot derivatives, may intrinsically modulate macrophage behavior, we conducted a comprehensive screening assay to characterize the global macrophage response to PRF exposure. To this end, we employed two widely used monocytic cell lines-U937 (histiocytic lymphoma) and THP-1 (acute monocytic leukemia)-as models to investigate macrophage responses. Cells were exposed to lysates derived from PRF, and transcriptomic alterations were profiled using bulk RNA sequencing. Differential gene expression analysis was performed, with significance determined by an adjusted p-value threshold of <0.05. In U937-derived macrophages, gene expression profiling revealed a transcriptional signature consistent with inflammatory activation. Clustering of upregulated genes highlighted pathways associated with chemokine activity (e.g., CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL20, CCL23, CCL26, CXCL5, CXCL6, CXCL8, CXCL16, and PPBP), RAGE receptor binding (FPR1, S100A8, S100A9, and S100A12), IgG binding (FCGR1A, FCGR2A, FCGR2B, and FCGR3A), prostaglandin biosynthesis (CBR1, CD74, EDN1, FABP5, IL1B, MIF, PTGES, and PTGS1), and collagen catabolism (CTSL, FAP, MMP3, MMP7, MMP9, MMP12, MMP14, MMP19, and MRC2). In contrast, PRF exposure in THP-1 cells primarily enriched genes involved in steroid biosynthesis, suggesting a more limited or distinct response. These findings underscore U937 cells as a more responsive and appropriate bioassay for modeling inflammatory macrophage polarization in response to PRF. Moreover, the identified gene signatures recapitulate key aspects of early wound healing, providing a relevant platform for studying macrophage reactivation in chronic wound environments. - Source: PubMed
Publication date: 2026/04/22
Panahipour LaylaHuang XiaoyuZampino FrancescaMiron Richard JGruber Reinhard - The pathogenic bacterium is a major cause of antibiotic-associated diarrheal disease. Treatment of the disease is challenging because antibiotics used for treatment may also perpetuate the conditions that contributed to initial susceptibility. Elucidating the mechanisms of /intestinal epithelium interaction is needed to facilitate the development of new therapeutic options. The studies described in this communication demonstrate the development of a tissue culture system that supported the growth of in co-culture with a model of the human intestinal epithelium produced from colonoids, organoids derived from human colonic biopsies. Epithelial cell responses to included upregulation of , encoding a chemokine. Glucosylating toxin production by the bacteria was required for upregulation of CCL20. Additionally, bacteria associated with the monolayer in a non-toxin dependent manner. This system will support future investigation of epithelium/ interactions during CDI and identification of mechanisms that drive pathogenesis by in the human intestine. - Source: PubMed
Publication date: 2026/04/29
Zucchi PaolaGladden Adrianne DDay Andrew WDressler JulesGovind RevathiAlmeqdadi MohammadRoper JatinTai AlbertBatorsky RebeccaKumamoto Carol A