CXCL5
- Known as:
- CXCL5
- Catalog number:
- 000662A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CXCL5
Related genes to: CXCL5
- Gene:
- CXCL5 NIH gene
- Name:
- C-X-C motif chemokine ligand 5
- Previous symbol:
- SCYB5
- Synonyms:
- ENA-78
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-09-03
- Date modifiied:
- 2016-10-24
Related products to: CXCL5
Related articles to: CXCL5
- 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 - Circadian rhythm disruption has been associated with the exaggerated inflammatory responses in peripheral tissues; however, its impact on neuroinflammation and blood-brain barrier (BBB) integrity remains unclear. Here, we identify the astrocytic circadian clock as a key regulator of BBB homeostasis during systemic inflammation. In a mouse model, circadian rhythm disruption for three weeks markedly increased BBB permeability in male mice, as evidenced by Evans blue leakage and myeloid cell infiltration into the brain parenchyma following lipopolysaccharide (LPS) challenge. Transcriptomic analyses using public datasets revealed that astrocytes exhibit the highest expression of core circadian clock genes among brain cell types. Accordingly, we generated tamoxifen-inducible, astrocyte-specific Bmal1-knockout (KO) mice. Deletion of Bmal1 in astrocytes significantly enhanced BBB leakage, astrogliosis and pericyte loss after LPS administration. Mechanistically, Bmal1-deficient astrocytes produced elevated levels of the chemokine CXCL5, which promoted CXCR2-dependent neutrophil recruitment into the brain. Pharmacological blockade of CXCR2 with SB225002 restored pericyte coverage and attenuated BBB disruption in astrocytic Bmal1 KO mice. Functionally, these mice exhibited impaired excitatory synaptic transmission following systemic inflammation, suggesting that astrocytic Bmal1 loss compromises neurovascular and synaptic integrity. Taken together, our findings demonstrate that astrocytic Bmal1 maintains BBB integrity and synaptic stability under inflammatory stress. This work also highlights astrocyte-intrinsic circadian regulation as a critical mechanism linking chemokine production to neurovascular vulnerability. - Source: PubMed
Publication date: 2026/05/06
Lee ChangjunLee YelinJeong Woo ChanHwang InhwaBae HarinShim Do-WanJung HyejiUm Ji WonYu Je-Wook - Here, we examine immune signaling pathways affecting the duration of primary nasopharyngeal colonization by Streptococcus pneumoniae (Spn), the first step in its pathogenesis. Spn colonization which lasts days to weeks in WT mice was persistent (> 6 months) in the absence of IL-17RA-signaling. RNA-seq analysis confirmed the role of IL-17RA signaling in neutrophil-associated pathways. The onset of clearance required neutrophils, but there was no detectable increase in their numbers. IL-17RA-signaling was required to replenish neutrophils in nasal tissue that were otherwise depleted during infection. Enhanced neutrophil trafficking correlated with IL-17RA-dependent expression of endothelial cell adhesion molecules that promote neutrophil trafficking from the circulation into nasal tissue. Persistent colonization was also observed in mice lacking IL-1R-signaling. Recognition of IL-1-family cytokines, however, was not necessary for the expression of IL-17A or neutrophil recruitment. Instead, IL-1R-signaling was associated with the activation of neutrophils in nasal tissue that displayed increased levels of the surface marker CD11b, an important receptor for the complement-opsonized phagocytosis of Spn. Colonization of dual-knockout mice showed the contributions of IL-1 and IL-17 signaling pathways were non-redundant. Expression of the chemokine Cxcl5 was impaired in the absence of either IL-1R or IL-17RA signaling, suggesting a role in both activation and maintenance of the neutrophil population during infection. Our findings provide insight into the requirement for sustained neutrophil presence and activity to prevent persistent mucosal infection by a leading opportunistic mucosal pathogen. - Source: PubMed
Publication date: 2026/05/05
Idowu TeniolaLokken-Toyli KristenYeung StephenWeiser Jeffrey N - This study aimed to investigate the systemic immune landscape in patients experiencing urogynaecological mesh failure. The use of urogynaecological mesh was paused in the UK following an independent safety review that found ~1 in 15 women required removal due to complications. However, the mechanisms underpinning mesh failure remain largely unknown, with few studies focussing on localised tissue responses and no reports characterising systemic immune dysregulation. - Source: PubMed
Publication date: 2026/04/30
Jamieson ShannonDougan Cameron RRennie EloiseCard PatrickNallappa SudarshanSmith KarenDeehan David JBrown KarenHilkens Catharien M UHarding Christopher - CXCL5 is an epithelial cell-derived neutrophil-activating peptide implicated in intestinal inflammation. We investigated the role of CXCL5 in inflammatory bowel disease (IBD), with a focus on its interaction with IL-17 signaling. CXCL5 expression in colonic tissues from patients with IBD and its association with clinical disease activity were analyzed. Publicly available single-cell RNA sequencing data were examined to identify CXCL5-expressing cell populations. Acute and chronic murine colitis models were used to assess the functional role of CXCL5 in vivo, and cytokine expression was evaluated. In vitro experiments were performed in human intestinal epithelial cells to examine CXCL5 regulation by inflammatory cytokines. CXCL5 expression positively correlated with fecal calprotectin levels in IBD patients and was significantly reduced in ulcerative colitis patients achieving endoscopic mucosal healing. Single-cell analysis revealed CXCL5 expression concentrated in a discrete epithelial cluster. IL17RA was broadly expressed across epithelial and immune cell populations, including the CXCL5-expressing epithelial subset, which may suggest the capacity of these cells to respond to IL-17A signaling. In acute DSS-induced colitis, CXCL5 deficiency markedly attenuated inflammation and neutrophil recruitment, accompanied by reduced IL-17A expression. Conversely, CXCL5 deficiency did not significantly alter disease severity in chronic colitis models. In vitro, TNF-α induced CXCL5 expression, which was further enhanced by IL-17A. CXCL5 contributes to neutrophil-driven intestinal inflammation in a phase-dependent manner and the CXCL5/IL-17 axis may represent a potential therapeutic target, warranting further mechanistic investigation. - Source: PubMed
Publication date: 2026/04/29
Moon Jung MinLim EunsuMin HyeyoungKim Kwang WooPark HyunsunKoh Seong-JoonKim Joo Sung