Rat MIP-3a ELISA kit
- Known as:
- Rat MIP-3a Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- LF-EK50673
- Product Quantity:
- 1
- Category:
- Elisa Kits
- Supplier:
- Abfron
- Gene target:
- Rat MIP-3a ELISA kit
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- Periodontitis, caused by the oral pathobiont Porphyromonas gingivalis (Pg), leads to progressive systemic diseases through oral-organ interactions, including cognitive dysfunction. However, the behavioral and immunological mechanisms underlying the oral-brain axis during the development of periodontitis remain unclear. We found that Pg-induced periodontitis promoted anxiety-like behavior and progressive cognitive dysfunction in mice. While Pg-induced periodontitis drove the accumulation of interleukin (IL)-17A-producing T cells in the mouth, an increased population of Vγ4 γδ T cells migrate to the brain through the draining cervical lymph nodes via the CCL20/CCR6 pathway. Treatment with an anti-IL-17A antibody, an anti-CCL20 antibody, or anti-TCRγδ antibody ameliorated both anxiety-like behavior and cognitive dysfunction, and suppressed the increased expression of IL-17A receptor in the brain. Collectively, our findings reveal a function beyond its established role for IL-17A in the oral-brain axis that links Pg-induced periodontitis to cognitive dysfunction. - Source: PubMed
Publication date: 2026/08/27
Kishikawa SariNagao Jun-IchiToyonaga KenjiIwanuma AobaIwai SatoruAosaka ArisaTanaka Yoshihiko - The inflammatory response is central to the pathogenesis of alcohol-associated liver disease (ALD), yet currently used prognostic scores, including Maddrey's modified discriminant function (mDF), Child-Turcotte-Pugh (CTP), MELD-Na and MELD 3.0, reflect hepatic synthetic and excretory function rather than the underlying immune alterations. Since CC-motif chemokines (CCLs) regulate immune cell trafficking and hepatic stellate cell activation, they warrant deeper investigation, as reports on their role in ALD remain limited. Therefore, the primary objective of this study was to evaluate the diagnostic and prognostic performance of selected serum CCLs, and to correlate their levels with disease severity and short-term survival in patients with ALD. Serum MIP-3α/CCL20, MCP-1/CCL2 and TARC/CCL17 were measured in 63 patients with ALD and 25 healthy controls using ELISAs. Chemokine concentrations were correlated with liver function tests, inflammatory indices and short-term (30-day) survival. The diagnostic and prognostic performances of individual CC chemokines were assessed by ROC analysis and by univariate and multivariable logistic regression. MIP-3α/CCL20 was increased more than 11-fold in ALD versus healthy controls and reached an AUC of 0.978 for distinguishing the two groups in a case-control comparison (a proof-of-principle, case-control result which requires validation against other chronic liver diseases). It increased across Child-Turcotte-Pugh classes and correlated with all other prognostic scales. MCP-1/CCL2 was significantly elevated in the ALD group but did not discriminate ALD severity. TARC/CCL17 was significantly lower in ALD than in controls. On multivariable regression, MIP-3α/CCL20 was the dominant predictor of both ALD status and severe liver dysfunction. In patients with ALD, MIP-3α/CCL20 appears to bridge hepatic inflammation and hepatocellular failure and is a candidate exploratory biomarker of disease severity that requires further confirmation against other chronic liver diseases. The short-term mortality analysis was based on only seven events. This evaluation is exploratory and underpowered, and its findings should not be interpreted as definitive prognostic evidence. MCP-1/CCL2 does not stratify ALD severity. Decreased TARC/CCL17 concentrations point to a separate immunoregulatory failure and are presented as a hypothesis requiring mechanistic testing in pre-clinical models. - Source: PubMed
Publication date: 2026/08/10
Szczerbinska AgnieszkaRolinski JacekSurdacka AgataCichoz-Lach Halina - Colitis-associated colorectal cancer (CAC) exemplifies how chronic intestinal inflammation can be converted into sustained epithelial programs and a permissive tumor microenvironment, yet the molecular linkage between inflammatory cytokine cues and chemokine outputs remains incompletely defined. Here, we identify a TNF-α-responsive YAP1-CCL20 program in colorectal inflammation and cancer. Across public cohorts and clinical specimens, YAP1 was elevated in ulcerative colitis and colorectal cancer and positively correlated with TNF-α expression. TNF-α increased YAP1 mRNA in both NCM460 and HCT116 cells. In HCT116 cells, TNF-α also increased YAP1 protein abundance and promoted its nuclear accumulation, whereas infliximab attenuated TNF-α-induced YAP1 mRNA and protein upregulation. Transcriptomic profiling following YAP1 silencing highlighted CCL20 among the most markedly downregulated genes. YAP1 gain- and loss-of-function consistently regulated CCL20 expression and secretion, and mechanistic assays demonstrated that YAP1/TEAD activity directly transactivated the CCL20 promoter. Functionally, TNF-α enhanced proliferation, migration, and invasion of colorectal cancer cells, effects that were blunted by YAP1 knockdown; CCL20 overexpression partially rescued the suppressed malignant phenotypes caused by YAP1 silencing. In vivo, verteporfin and/or infliximab ameliorated DSS-induced colitis, accompanied by reduced colonic Yap1 and Ccl20 expression, lower serum CCL20, and diminished mucosal accumulation of CD3⁺ T cells, CD19⁺ B cells, CD11c⁺ dendritic cells, and FOXP3⁺ regulatory T cells. Moreover, combined YAP pathway inhibition and CCL20 knockdown produced the most pronounced suppression of xenograft tumor growth. Together, these findings position CCL20 as a mechanistically defined downstream effector of YAP1 and suggest that a TNF-α-responsive YAP1-CCL20 program contributes to inflammatory chemokine remodeling in colitis and to malignant phenotypes of colorectal cancer cells. - Source: PubMed
Publication date: 2026/08/10
Chen LibinAi FeiyanYu WentaoXiang BoShen ShourongMa JianLi Xiayu - Triple-negative breast cancer (TNBC) derives limited benefit from immune checkpoint blockade, largely owing to primary resistance shaped by the tumor immune microenvironment. Here, baseline transcriptomic profiling of a neoadjuvant chemoimmunotherapy cohort identified carbohydrate sulfotransferase 1 (CHST1) as a candidate resistance-associated gene. High CHST1 expression was associated with poor immunotherapy response and inferior clinical outcome across clinical datasets. Functionally, CHST1/Chst1 had minimal effects on tumor-cell-intrinsic proliferation, migration, or invasion in vitro, but promoted tumor growth in an immune context-dependent manner in vivo. Mechanistic analyses support a model in which CHST1 associates with NF-κB-repressing factor (NKRF) and limits its nuclear accumulation, a localization change associated with increased NF-κB-related CCL20 expression. Tumor-cell CCL20 perturbation and rescue experiments further supported a functional contribution of CCL20 to macrophage recruitment and M2-like remodeling. Pharmacologic CCR6 blockade enhanced the antitumor activity of anti-PD-1 therapy in syngeneic TNBC models. Finally, a CHST1-NKRF-CCL20 expression signature showed potential value for stratifying immunotherapy response. Collectively, this study supports a CHST1-NKRF-CCL20 regulatory model and identifies CCR6 blockade as a potential therapeutic strategy. - Source: PubMed
Publication date: 2026/08/24
Jiang Shu-HaoYing Xiao-HanWang Ruo-QingZhang QunChen LiShao Zhi-MingLi Jun-Jie - Multiple sclerosis (MS) is treated with branded or generic disease-modifying therapies (DMTs), with increasing concern for the composition and quality of off-patent products. Our objective was to evaluate differences in disease-specific biomarkers, a potential indicator of suboptimal therapeutic exposure, between individuals treated with branded and generic DMTs. We compared biomarker variability in MS individuals (n=1,124) treated with generic or brand-name fumarates (diroximel fumarate, dimethyl fumarate (DMF)), fingolimod, and teriflunomide. In the generic DMF group, higher coefficients of variation (COV) for CXCL9, CCL20, and TNFSF13B were observed, with a paradoxically lower variability for CXCL13. Higher COVs for CXCL9 were observed with generic fingolimod and for CXCL9 and CXCL13 with generic teriflunomide when compared to brand. Additionally, all generic DMTs demonstrated higher multi-variable variability index values across 18 proteins associated with MS disease activity. Greater biomarker variability with generic formulations may reflect differences in therapeutic exposure and less consistent disease control. - Source: PubMed
Publication date: 2026/08/23
Okuda Darin TAnderson Benjamin JTaylor Sophia MJones-McCreary Morgan CBurgess Katy WWright Crystal MSantoyo Jose RSguigna Peter VStüve OlafTran Diem HLight David YMoog Tatum MPunnen Tom G