Anti_Mouse, mab CXCL2 Source Rat
- Known as:
- Anti_Mouse, mab CXCL2 Source Rat
- Catalog number:
- 103-M360
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Mouse mab CXCL2 Source Rat
Related genes to: Anti_Mouse, mab CXCL2 Source Rat
- Gene:
- CXCL2 NIH gene
- Name:
- C-X-C motif chemokine ligand 2
- Previous symbol:
- GRO2
- Synonyms:
- SCYB2, GROb, MIP-2a, MGSA-b, CINC-2a
- Chromosome:
- 4q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-05-21
- Date modifiied:
- 2016-10-24
Related products to: Anti_Mouse, mab CXCL2 Source Rat
Related articles to: Anti_Mouse, mab CXCL2 Source Rat
- Poor air quality, and particularly particulate matter (PM), is detrimental to health, contributing to chronic inflammatory conditions and worsening the outcomes to infections. PM has major impacts on barrier tissues including the lungs, gut, and skin. These tissues are lined by epithelial cells that can initiate and contribute to immune responses, but we still do not fully understand how they respond to PM. Furthermore, PM is multifactorial, and which components may be the most triggering for immune responses are not known. We evaluated the impact of a range of PM components including transition metals and components of diesel exhaust particulates (DEP) on lung-, gut-, and skin-derived epithelial cells. Differences in toxicity were observed between components, with the polyaromatic hydrocarbon 1, 2-naphthoquinone extremely toxic at concentrations of 100 μg/mL, contrasting with 2-nitrofluorenone and 2-methyl-4-nitrophenol. At lower nonlethal concentrations, 1, 2-naphthoquinone promoted epithelial cell production of the chemokines CXCL1 and CXCL2 that are associated with neutrophil recruitment, contrasting with other pollutants evaluated. Furthermore, 1, 2-naphthoquinone caused broad transcriptional changes in the lung epithelial cells. These results highlight the potential dangers of discrete components of PM such as 1, 2-naphthoquinone on epithelial function, indicating the potential to alter the immune landscape in the lung. - Source: PubMed
Publication date: 2026/06/18
Adams GeorgeWagstaff OliverTopping DaveBrough DavidLopez-Castejon GloriaD'Elia RiccardoCruickshank Sheena M - Background Metabolic disorders associated with elevated saturated fatty acids are linked to chronic inflammatory diseases, including periodontitis, yet the mechanisms connecting lipotoxic stress to gingival inflammation remain unclear. This study investigated how palmitate-induced metabolic stress affects purinergic signaling, mitochondrial function, and endoplasmic reticulum (ER) stress in murine gingival fibroblasts (mGF), and whether adenosine modulates these effects. Methods mGF were treated with BSA control, palmitate, IL-1β, or palmitate plus IL-1β, followed by bulk RNA sequencing, Seahorse metabolic analysis, biochemical assays, and transmission electron microscopy. Results Palmitate suppressed expression of key adenosine-generating ectoenzymes and purinergic signaling genes, including Cd73 (Nt5e), Cd39 (Entpd1), Adk, Ada, and adenosine receptors. Concurrently, palmitate amplified IL-1β-induced inflammatory mediators such as Cxcl1, Cxcl2, Cxcl5, Ccl2, and Il6. Gene ontology analysis demonstrated enrichment of pathways related to innate immune activation, oxidative stress, mitochondrial dysfunction, ER stress, and purine metabolism. Palmitate also induced intracellular lipid accumulation and mitochondrial dysfunction, evidenced by reduced NAD+/NADH ratio, increased mitochondrial reactive oxygen species (ROS), elevated protein oxidation, and increased proton leak despite enhanced electron transport chain protein expression. Ultrastructural analyses revealed swollen mitochondria, ER expansion, and increased ER-mitochondrial associations. Mechanistically, palmitate activated the Perk-eIF2α-Atf4 ER stress pathway, increasing phosphorylation of Perk and eIF2α and elevating Atf4 expression. Extracellular adenosine attenuated mitochondrial ROS accumulation, reversed Perk and Atf4 activation, improved mitochondrial respiration, and preserved ER and mitochondrial ultrastructure. Conclusions Palmitate disrupts the Cd73-adenosine axis while promoting mitochondrial dysfunction, oxidative stress, and Perk-mediated ER stress in gingival fibroblasts. Adenosine signaling protects against lipotoxic-induced ER stress, highlighting the Cd73-adenosine pathway as a potential therapeutic target in metabolically driven periodontal inflammation. - Source: PubMed
Publication date: 2026/06/15
Dawson ShantieceBatan SoniaAdams NinaBombin SergeiRamos-Junior Erivan SMorandini Ana Carolina - Metastases are a primary cause of cancer-associated mortality; however, the mechanisms underlying aggressive progression have not been clearly elucidated. Genome-wide features of chromatin accessibility through ATAC-seq from HCC primary and metastatic tumors revealed that many distal regulatory elements spreading the genome become accessible during aggressive progression, the changes of which are associated with NFY-family. And NFYB is frequently upregulated in tumor with metastasis. Mechanistically, LINC01137 recruits SMYD3 to enhance H3K4me3 occupancy at IL-1, CXCL2 and CCL20 promoters by inhibiting lysine ubiquitination to stabilize NFYB, which in turn upregulates IL-1, CXCL2 and CCL20. HCC-derived cytokine transforms macrophages to the M2 phenotype to foster an inhibitory tumor microenvironment and anti-PDL1 tolerance. Importantly, LINC01137 transcription is activated by the NFYB/KAT2B complex in a feed-forward loop. Notably, treatment with an IL-1 inhibitor enhances the blockade efficacy of PD-L1 in NFYB-overexpressing HCC. Our findings imply an immunosuppressive role of NFYB-LINC01137 signaling during aggressive HCC progression and support the concept of microenvironment engineering in immunotherapy. - Source: PubMed
Publication date: 2026/03/25
Zhou BoxuanTao QiangWen WuTan JiananXu JieFang YixuanGuan JiaoLin XiaorongHe JiehuaAshrafizadeh MiladWang ZifengConde JoãoZheng Fang - Ulcerative colitis (UC) is a chronic inflammatory bowel disease marked by immune cell infiltration, crypt erosion, and severe ulceration. In phase 3 studies with etrolizumab, the results of a transcriptional analysis of colonic biopsies revealed that etrolizumab-mediated integrin β7 blockade, but not adalimumab (a TNF-blocking antibody), reduced genes associated with integrin αEβ7+ intraepithelial lymphocytes (IELs). Both treatments significantly reduced stromal and myeloid cell-related genes linked to Mayo Clinic Score (MCS) remission status. A single-cell atlas from UC biopsies identified 36 distinct cell populations, including myeloid cells. This atlas enabled cell-specific signatures and cellular deconvolution of the phase 3 data, showing reductions in neutrophils, monocyte-derived macrophages, and inflammatory fibroblasts, along with increases in epithelial cells common to both treatments. Pseudo-time analyses identified four neutrophil subsets, transitioning from PADI4hi, OSMhi, and MX1hi to CXCR4hi populations. PADI4hi and OSMhi neutrophils exhibited high protease, cytokine (CXCL1, IL1B, OSM), and chemokine receptor (CXCR1, CXCR2) levels, while MX1hi expressed markers of IFN exposure. CXCR4hi neutrophils showed elevated CXCL2, TNF, and VEGFA levels. Notably, interactions between PADI4hi and OSMhi neutrophils and inflammatory fibroblasts, such as OSM and IL1B, were associated with MCS remission with both drugs. CXCR4hi neutrophils showed only minor changes unrelated to clinical outcomes. These findings suggest that neutrophils are highly heterogeneous, with abundant interactions in inflamed colonic tissue, potentially perpetuating chronic disease. Disrupting neutrophil interactions with myeloid and resident cells like inflammatory fibroblasts could reduce inflammation, possibly enhancing clinical remission rates. - Source: PubMed
Publication date: 2026/06/11
Eshghi Shadi ToghiGubatan John MarkMazrooei ParisaQuintanilla LuisNguyen AllenAu-Yeung AmeliaHolman Derek RTakahashi ChikaraSchiffman CourtneyO'Gorman William EKeir Mary ERamanujan SarojaRogalla StephanHackney Jason AMcBride Jacqueline M - Candida auris (C. auris) is an emerging fungal pathogen with a remarkable ability to persist on human skin, but how structural skin cells respond to colonization is unclear. We used ex vivo human skin models, together with primary keratinocytes and fibroblasts, to characterize epithelial and stromal responses to C. auris compared with Candida albicans. C. auris formed biofilms and induced a wound-model-dependent pattern of cytokine secretion dominated by IL-1β and IL-6, yet caused minimal epithelial damage and modest reductions in leukocyte viability. RNA sequencing revealed complementary but cell-type-specific responses. Keratinocytes and fibroblasts both amplified a pro-inflammatory IL-6/CXCL8 response, while keratinocytes additionally upregulated antimicrobial genes such as RNASE7, TSLP, DEFB103A (encoding hBD-3), and the neutrophil-recruiting chemokines CXCL2 and CXCL3. Fibroblasts further induced CCL28, supporting T cell recruitment, alongside transcriptional programs associated with tissue remodeling. Recombinant RNase 7 and short form TSLP directly inhibited C. auris growth in vitro in a dose-dependent manner. Together, these findings identify keratinocytes as epithelial sentinels that integrate inflammatory and antimicrobial defenses against skin-tropic C. auris and suggest that fibroblast-driven cytokine amplification and especially antimicrobial peptides from within the skin barrier may provide therapeutic targets to limit C. auris skin colonization. - Source: PubMed
Publication date: 2026/06/26
Seiser SaskiaBrezovec HelenaPenninger PhilippPhan-Canh TrinhMoser DorisAssen Frank PAyub TanyaRademacher FranziskaGläser RegineCerbu DianaKienzl PhilipFreystätter ChristianHarder JürgenKuchler KarlElbe-Bürger Adelheid