ENA-78 CXCL5 (5-78a.a.), Human
- Known as:
- ENA-78 CXCL5 (5-78a.a.), Human
- Catalog number:
- Z02820-20
- Product Quantity:
- 20,0μg
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- ENA-78 CXCL5 (5-78a..) Human
Related genes to: ENA-78 CXCL5 (5-78a.a.), Human
- 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: ENA-78 CXCL5 (5-78a.a.), Human
Related articles to: ENA-78 CXCL5 (5-78a.a.), Human
- 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 - In this exploratory study with a limited sample size, we aimed to investigate inflammation-related proteins in the aqueous humor of high myopia (HM) patients, analyze their correlations with ocular parameters, and screen for potential biomarkers. - Source: PubMed
Publication date: 2026/06/23
Yang MingWu WeizhenDong NingLi Min - [This retracts the article DOI: 10.3727/096504016X14732772150343.]. - Source: PubMed
Publication date: 2026/06/16
- Enhancing innate-adaptive immune crosstalk is key for improving cancer vaccine efficacy. TRIMELVax is a heat shock-conditioned whole-tumor-cell vaccine combining xenogeneic melanoma cell lysate, syngeneic B16F10 melanoma cell lysate, and hemocyanin. Although TRIMELVax elicits robust antitumor responses in preclinical models, the mechanisms underlying its efficacy remain poorly defined. We characterized the early immune events triggered by TRIMELVax in mice using RT-qPCR, high-dimensional flow cytometry, immunohistochemistry, CFSE-based dendritic cell (DC) migration assays, and therapeutic melanoma models with transient neutrophil depletion. TRIMELVax elicited a rapid inflammatory response at the vaccination site, characterized by local upregulation of , and . This response drove an early influx of neutrophils and monocytes, followed by increased accumulation of cDC1, cDC2, and monocyte-derived DCs. Notably, we identified a transient population of neutrophils expressing markers associated with antigen-presenting cells (CD45⁺, CD11b⁺, Ly6G⁺, CD11c⁺, MHC-II⁺) that emerged within 12-24 hours postvaccination. These APC-like neutrophils colocalized with cDC1 at the injection site and subsequently migrated to the popliteal draining lymph nodes (pLN). Neutrophil depletion impaired cDC1 migration, reduced APC accumulation in pLN, and abolished the therapeutic efficacy of TRIMELVax. Together, these findings identify neutrophils as key early regulators of the innate inflammatory environment induced by TRIMELVax and suggest that neutrophils with APC-like features may impact DC trafficking and downstream antitumor immunity. Neutrophils, particularly those with APC-like phenotypes, emerge as promising cellular adjuvant targets for enhancing cancer vaccination strategies, offering a new avenue for rational vaccine design and combination with checkpoint blockade therapies. - Source: PubMed
Publication date: 2026/06/25
Pérez-Baños AmarilisGleisner María AlejandraTittarelli AndrésTapia DanielaCuevas María ElisaMardonez AntoniaTempio FabiánAstaburuaga-García RosarioFlores IvánPereda CristianLladser ÁlvaroGonzález Fermín EValenzuela SebastiánRicca MicaelaBecker María InésBlüthgen NilsAchour AdnaneSalazar-Onfray Flavio - Neurosyphilis has resurged globally, presenting a significant public health threat, yet challenges in early diagnosis persist. This study aims to evaluate the diagnostic value of C-X-C motif chemokine ligand 1 (CXCL1), C-X-C motif chemokine ligand 5(CXCL5), and C-X-C motif chemokine ligand 8 (CXCL8) in cerebrospinal fluid (CSF) for neurosyphilis. - Source: PubMed
Publication date: 2026/06/03
Zhang YanJin YujiaoLiu YuanXue LizhiGu KailongDu WeiLiu ShourongXu Aifang