Eotaxin _ CCL11
- Known as:
- Eotaxin _ CCL11
- Catalog number:
- PA1140
- Product Quantity:
- 2 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- Eotaxin _ CCL11
Related genes to: Eotaxin _ CCL11
- Gene:
- CCL11 NIH gene
- Name:
- C-C motif chemokine ligand 11
- Previous symbol:
- SCYA11
- Synonyms:
- eotaxin, MGC22554
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-24
- Date modifiied:
- 2016-10-05
Related products to: Eotaxin _ CCL11
Related articles to: Eotaxin _ CCL11
- Adult hematopoietic stem cells (HSCs) and bone marrow (BM) mesenchymal stem/stromal cells (MSCs) are essential for lifelong hematopoiesis, skeletal homeostasis, immune competence, and tissue regeneration. The use of electronic cigarettes (E-cigs) among women of reproductive age continues to rise, raising concerns about potential adverse developmental effects; however, the long-term consequences of maternal E-cig vaping on offspring BM stem cell function and hematopoietic homeostasis remain incompletely understood. Here, using a rat model of maternal E-cig exposure (containing nicotine) during gestation, combined with longitudinal in vivo analyses and complementary ex vivo studies of human cells, we show that prenatal E-cig exposure is associated with persistent alterations in offspring BM stem cell function and lineage commitment. Gestational E-cig exposure was associated with expansion of the CD11b/c myeloid-enriched compartment, increased CD90 stromal cells, and impaired osteogenic differentiation in rat offspring. Complementary experiments using primary human cells showed that nicotine exposure was associated with reduced T-cell proliferation and impaired cytotoxic activity in a proof-of-principle co-culture assay. Mechanistically, transcriptomic profiling followed by Gene Ontology and pathway enrichment analyses identified alterations in molecular programs associated with KLF4-Notch1 signaling, mitochondrial biogenesis, inflammation, and stem cell regulation in the BM of E-cig-exposed rat offspring. Changes in CCL11, FTO, and RUNX2 were additionally associated with an inflammatory and aging-related molecular phenotype that persisted from early life into adulthood, although these findings do not establish a causal CCL11-FTO-RUNX2 signaling axis or direct cellular senescence. Collectively, our study provides a phenotypic and mechanistic framework for understanding how maternal E-cig exposure may influence long-term offspring hematopoietic, skeletal, and immune health while highlighting the need for further studies to establish causal molecular mechanisms and determine their relevance to maternal E-cig use in humans. - Source: PubMed
Publication date: 2026/08/24
Xiao JeffreyPark BrandonLi YongWasnik SamikshaFattah Farzad DanielLee ScottCodorniz KevinTan LarenChang AndrewSaca LuisMoreno Pamela LoboMatus MichaelMirshahidi SaiedNarayan Raja RSaid Hamid MMirshahidi HamidReeves Mark EAbdel-Azim HishamCao HuynhMohan SubburamanBaylink David JXu Yi - Juvenile colorectal polyps (JP) are the most common polypoid lesions of the colon in children and the leading cause of lower gastrointestinal bleeding in pediatric patients. Although histologically classified as benign hamartomatous lesions, they arise in a context of allergic sensitization and IgE-mediated inflammation, suggesting that the epithelial compartment may play an active role in their pathogenesis. To date, most studies have focused on the immune cell infiltrate, leaving the molecular programs operating within the epithelium largely unexplored. Whole-transcriptome RNA sequencing (RNA-seq) was performed on epithelial cells isolated from pediatric JP ( = 8) and paired tissue circumjacent to polyp (TCP) ( = 7) obtained from children with a history of rectal bleeding and IgE sensitization to food allergens. Differential expression, functional enrichment (GO, KEGG, GSEA), and cross-dataset comparison with TCGA colorectal adenocarcinoma (CRC) was conducted. Candidate genes were validated by RT-qPCR in independent samples, including colorectal cancer (CRC) and inflammatory bowel disease (IBD) tissue. Differential expression analysis identified 3273 differentially expressed genes (2342 upregulated, 931 downregulated in JP vs. TCP), with 220 genes exceeding 32-fold change, including (log2FC = 12.16), (log2FC = 10.19), (log2FC = 10.08) and (log2FC = 8.87). JP epithelium displayed a coherent type 2 inflammatory signature, encompassing upregulation of the alarmin IL33, eosinophil-attracting chemokines (, ), IgE receptor subunits (, ), and a coordinately activated leukotriene and prostaglandin biosynthetic program (, , ). Concurrent alterations in epithelial identity were observed, including downregulation of absorptive enterocyte and intestinal stem cell markers (, , ) alongside upregulation of secretory and regenerative programs, including the ectopic gastric-type mucin . Tight junction dysregulation-notably upregulation of the pore-forming claudin and loss of barrier-sealing claudins (, , )-was consistent with impaired epithelial permeability. Pathway analyses confirmed activation of type 2 immune and extracellular matrix remodeling programs, with concurrent suppression of mitochondrial oxidative phosphorylation. Cross-dataset comparison with TCGA CRC data identified 381 co-upregulated and 87 co-downregulated genes shared between JP and CRC, including , , , and , several of which were associated with poorer disease-specific survival in CRC patients. RT-qPCR validation confirmed elevation of and in both JP and CRC, while appeared JP-specific. Epithelial cells from pediatric juvenile colorectal polyps associated with allergic sensitization display a comprehensive type 2 inflammatory transcriptome alongside profound alterations in lineage identity, barrier integrity, and metabolic programming. Partial convergence with CRC-associated gene expression programs-in the absence of histological dysplasia-suggests that chronic allergic inflammation activates conserved epithelial remodeling pathways shared across mucosal tissues. , , and are candidate biomarkers warranting validation in larger cohorts. - Source: PubMed
Publication date: 2026/09/07
Polo María BelénIlid ManuelaBernedo VivianaBorobia PaulaMenendez LorenaZosi AnabellaZubirí CeciliaFernández Rivas MaximilianoRecalde María FlorenciaAguilar Becher Barbara VirginiaGarcía MarcelaAltamirano EugeniaGuzmán LucianaAbba MartinMuglia CeciliaDocena Guillermo - Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe autoimmune neurological disorder characterized by pathogenic antibodies against the NMDAR. A systematic protein profiling approach is warranted to identify biomarkers capable of predicting disease status. An Olink proximity extension assay (PEA) profiled 91 inflammation-related proteins from anti-NMDAR encephalitis patients. Disease severity or prognosis were assessed by CASE score or mRS score at 6-month follow-up. Patients were stratified into distinct molecular clusters using unsupervised clustering. Logistic regression models incorporating selected biomarkers were developed to predict disease severity and prognosis, followed by absolute quantification using ELISA. Patients were classified into four consensus clusters. Clusters 1 and 2 corresponded to the mild group, while Cluster 3 represented the severe group, consistent with CASE score above 6. Cluster 4 showed heterogeneous clinical features. Elevated serum levels of IL-10, IL-6, and SIRT2, as well as increased CSF levels of CXCL10, CXCL11, and MMP10, were positively associated with severe disease. Conversely, several proteins including LTA and CCL11, CCL8, TGFB1, CXCL6 were associated with severe disease or unfavorable 6-month outcomes. A logistic regression model combining serum CXCL6 and CCL11 with CSF MMP10 achieved an area under the curve (AUC) of 0.95 for predicting disease severity. Serum CCL11 alone showed predictive value for 6-month prognosis, with an AUC of 0.79. These findings delineate distinct protein signatures associated with clinical heterogeneity of anti-NMDAR encephalitis. Prediction models incorporating multiple biomarkers may provide an approach for disease severity stratification and prognosis forecast. - Source: PubMed
Publication date: 2026/08/24
Zhao ShufangXu FangCui LiliChen WeibiLiu GangZhang HuiminShan DaweiChai ShutingYang LeChai GuoliangWan DongshanZhang Yan - Chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by persistent mucosal inflammation and eosinophilic infiltration. Although epithelial and immune cells have been widely studied, the role of nasal fibroblasts in innate immune activation and eosinophil recruitment remains unclear. - Source: PubMed
Publication date: 2026/09/09
Shin ChaewonKim An-GiYu Byeong MinKwon Woo-KeunHwang Min-HoPark Joo-Hoo - : Chronic rhinosinusitis with nasal polyps (CRSwNP) is a heterogeneous type 2 inflammatory disease characterized by frequent postoperative recurrence despite endoscopic sinus surgery (ESS). Reliable biomarkers capable of predicting recurrence remain insufficiently validated. This study evaluates the prognostic utility of circulating biomarkers for recurrence prediction in CRSwNP, in addition to the predictive performance of the blood eosinophilia. : A prospective cohort of 69 patients with CRSwNP undergoing primary ESS was followed for up to 3 years. Periostin, eotaxin-3, procalcitonin and IL-33 were taken from blood before surgery and analyzed by ELISA technique. Clinical outcomes were assessed using SNOT-22 and Perioperative Sinus Endoscopy (POSE) scores. Statistical analyses included Spearman's correlation, the Mann-Whitney U test, the Kruskal-Wallis test, Cox proportional hazards regression, multivariable binary logistic regression, ROC analysis, and longitudinal MANCOVA. : Blood eosinophilia remained the strongest clinical predictor of recurrence (OR = 4.55, = 0.001). Serum periostin, eotaxin and procalcitonin significantly correlated with postoperative disease severity and recurrence, particularly with POSE scores at 1 and 3 years ( < 0.05). Patients with recurrence demonstrated significantly higher serum levels of these biomarkers compared with controlled patients (all < 0.001). Multivariate Cox regression identified periostin (HR = 1.033, = 0.010), eotaxin (HR = 1.554, < 0.001) and procalcitonin (HR = 1.183, < 0.001) as significant predictors of recurrence. Procalcitonin demonstrated the highest predictive performance in ROC analysis (AUC = 0.805). Longitudinal MANCOVA confirmed significant associations between periostin, eotaxin, procalcitonin, and persistent postoperative inflammatory burden over 3 years. : Circulating periostin, eotaxin and procalcitonin are promising predictors of CRSwNP recurrence and appear to contribute to prognostic accuracy. Integration of serum biomarker profiling into clinical practice may improve personalized postoperative management and risk stratification in CRSwNP. - Source: PubMed
Publication date: 2026/07/27
Florean Maria-DeliaMare CodruțaGâta AndaTrombitaș Veronica ElenaBudișan LiviuțaZanoaga OanaBerindan-Neagoe IoanaStelea Carmen GabrielaRoman AlexandraAlbu Silviu