TSLP_MOUSE Tslp ELISA tesk kit
- Known as:
- TSLP_MOUSE Tslp Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen17003
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- TSLP_MOUSE Tslp ELISA tesk kit
Related genes to: TSLP_MOUSE Tslp ELISA tesk kit
- Gene:
- TSLP NIH gene
- Name:
- thymic stromal lymphopoietin
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2007-08-24
- Date modifiied:
- 2014-11-18
Related products to: TSLP_MOUSE Tslp ELISA tesk kit
Related articles to: TSLP_MOUSE Tslp ELISA tesk kit
- Nasal epithelial barrier impairment is a crucial pathology in chronic rhinosinusitis with nasal polyps (CRSwNP). However, the mechanisms driving tight junctions (TJs) disruption remain unclear. We aimed to elucidate the role of IL-13 in TJs breakdown and epithelial remodeling, and to evaluate whether dupilumab can restore epithelial integrity under Type-2 inflammatory conditions. - Source: PubMed
Publication date: 2026/05/06
Huang Zhi-QunLiu JingSun Li-YingLuo QingYu Jie-QingShen LiXiong Yi-ShanYin Ran-RanWang De-YunYe Jing - Allergic rhinitis (AR) is a common chronic nasal mucosal inflammatory disorder driven by type 2 immunity, but the spatial stromal-immune cell interactions underlying its pathogenesis remain unclear. - Source: PubMed
Publication date: 2026/04/17
Zhao MiaoDuan JiaqiXie YongminHuang GuanYang GuiYang PingchangZeng Haotao - Thymic stromal lymphopoietin (TSLP) is central to the pathogenesis of atopic dermatitis (AD) and a promising therapeutic target. However, developing small-molecule TSLP inhibitors is challenging due to the difficulty in disrupting the TSLP-TSLPR interface. This study aimed to explore naturally sourced blockers of the TSLP-TSLPR interaction and identify novel candidate compounds for AD treatment. HuT78 cells were stimulated with PMA, ionomycin, and TSLP to establish an AD model. Inflammatory cytokines were measured by qRT-PCR and ELISA. JAK/STAT signaling was analyzed by Western blot. In female BALB/c mice, DNCB-induced AD-like skin lesions were topically treated with test compounds, followed by histopathological and immunohistochemical assessment. Eight compounds were screened, and their key structural features were elucidated via structure-activity relationship (SAR) analysis. Among them, kaempferol-7-O-glucoside (K-7-G) emerged as the most potent candidate. It interfered with the TSLP-TSLPR interaction, selectively inhibited TSLP-mediated JAK2/STAT5 phosphorylation, and significantly downregulated IL-4 ( < 0.0001) and IL-13 ( < 0.001) levels. Topical application of 1% K-7-G significantly alleviated AD-like symptoms in a mouse model, decreasing dorsal skin thickness, dermatitis score, and scratching frequency while restoring the expression of filaggrin, loricrin, and occludin ( < 0.0001). Meanwhile, it significantly reduced key inflammatory mediators in a concentration-dependent manner, including TSLP, IL-4, IL-13, TNF-α, IFN-γ, and IgE. This study demonstrates that K-7-G is a novel natural TSLP inhibitor capable of blocking the TSLP-TSLPR signaling pathway and effectively improving AD symptoms. Further research may explore its therapeutic potential in other inflammatory diseases. - Source: PubMed
Publication date: 2026/04/04
Lan XingmeiLiu JingShi YijieZhou YonghuaYang ChengZhao Bingtian - Atopic dermatitis (AD) is a chronic inflammatory dermatosis driven by skin barrier dysfunction, immune dysregulation, and gut-skin axis imbalance. While probiotics show promise, the therapeutic potential and mechanisms of topical postbiotics in modulating the gut-skin axis remain understudied. Here, we investigated the efficacy of -derived cell-free supernatant (CFS) and lysate (ShL) in a DNFB-induced AD mouse model. Topical application of both CFS and ShL significantly attenuated AD-like symptoms, reduced epidermal thickening, and restored the expression of the barrier protein filaggrin. Immunologically, treatment suppressed the Th2-dominant inflammatory cascade (IL-4, IL-5, IL-13, IL-33, TSLP) and reduced serum IgE and IFN-γ levels. Notably, ShL exhibited superior systemic efficacy, significantly inhibiting mast cell infiltration and reducing the spleen index. 16S rRNA sequencing revealed that topical intervention remotely remodeled the gut microbiota, specifically reversing the depletion of the beneficial genus and suppressing the compensatory increase in . This microbial restructuring was accompanied by distinct metabolic changes: ShL treatment resulted in an approximately 4-fold elevation in fecal butyrate concentrations compared with the model group. Correlation analysis further validated a strong positive axis linking abundance and butyrate levels to skin barrier integrity. Collectively, our findings demonstrate that postbiotics-particularly the lysate-ameliorate AD through a dual mechanism of local barrier repair and systemic metabolic modulation via the gut-skin axis, presenting a promising non-steroidal therapeutic strategy. - Source: PubMed
Publication date: 2026/04/17
Shi ZhijieLi KeLiang JiaqianYan LaifaGuo YuzhenLu ZhenmingZhang XiaojuanXu HongyuShi Jinsong - Severe asthma in routine practice often involves long-standing disease, multimorbidity, and prior biologic failure-settings underrepresented in pivotal tezepelumab trials. This study evaluated 52-week real-world effectiveness and safety of tezepelumab in a highly comorbid, predominantly T2-high, biologic-experienced severe asthma cohort from the Canary Islands. TEZNERIFE is a multicenter, retrospective study including consecutive adolescents and adults with GINA Step 5 severe uncontrolled asthma treated with tezepelumab 210 mg every 4 weeks for 12 months. Clinical outcomes, lung function, type 2 biomarkers, upper airway symptoms, and Biologics Asthma Response Score (BARS) were assessed at baseline, 26 weeks, and 52 weeks. Fifty-six patients (mean age 53.5 years, 71% female, mean asthma duration 30 years, 84% T2-high; 71% with ≥1 prior biologic) were analyzed. ACT improved from 11.5 ± 3.7 to 15.9 ± 4.7 at 26 weeks and 17.5 ± 4.7 at 52 weeks (both < 0.0001), while annualized exacerbations declined from 2.79 ± 2.0 to 0.50 ± 0.72 and 0.51 ± 0.89 (both < 0.0001). Maintenance oral corticosteroid dose fell from 10.2 ± 8.3 to 6.9 ± 2.4 mg/day at 52 weeks ( = 0.014). FEV1% predicted increased from 69.3 ± 19.2% to 75.3 ± 17.7% and 76.2 ± 20.6% ( = 0.004 and = 0.001), and blood eosinophils decreased from 234 ± 231 to 146 ± 120 and 147 ± 110 cells/µL ( = 0.001 and = 0.013). At one year, 18.9% and 67.9% were classified as good and intermediate responders by BARS; 13.2% were insufficient responders. Two patients discontinued due to non-serious adverse events, while no treatment-related serious events occurred. In this difficult-to-treat, multimorbid, biologic-experienced population, tezepelumab achieved sustained improvements in asthma control, exacerbations, lung function, eosinophilic inflammation, and corticosteroid exposure over 52 weeks, supporting upstream alarmin inhibition as a versatile strategy in complex severe asthma. - Source: PubMed
Publication date: 2026/04/09
González-Pérez RupertoDe Lorenzo-García IreneIzaguirre-Flores HemilyGonzález-Expósito HéctorGarcía Gil SaraPoza-Guedes Paloma