TLR4 pAb;mouse
- Known as:
- TLR4 pAb;mouse
- Catalog number:
- ASACSA-801E
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- TLR4 pAb;mouse
Related genes to: TLR4 pAb;mouse
- Gene:
- TLR4 NIH gene
- Name:
- toll like receptor 4
- Previous symbol:
- -
- Synonyms:
- hToll, CD284, TLR-4, ARMD10
- Chromosome:
- 9q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-25
- Date modifiied:
- 2016-01-21
Related products to: TLR4 pAb;mouse
Related articles to: TLR4 pAb;mouse
- - Source: PubMed
Publication date: 2026/04/30
Zhao Meng-QiJia Ju-FangLiu Tian-BoWang Wen-JieLiu Xue-QingWang Wen-FeiKuang Hai-XueLiang JunXia Yong-Gang - Antimicrobial resistance and dysregulated inflammation drive mortality in multidrug-resistant (MDR) sepsis. We evaluated the cationic peptide TP2-5 as a low-dose antibiotic adjuvant. At sub-MIC concentrations, TP2-5 enhanced antibiotic susceptibility of MDR E. coli in broth and 50% human serum, and in combination with antibiotics was associated with attenuated MIC escalation during 21-day serial passage. Membrane potential assays and cryo-electron tomography showed envelope perturbation characterized by inner-membrane hyperpolarization. This biophysical state was temporally associated with preferential interactions with lipopolysaccharide (LPS) and anionic phospholipids rather than nonspecific permeabilization. TP2-5 neutralized LPS and reduced TLR4-dependent cytokine production. In our murine polymicrobial CLP sepsis model, TP2-5 alone or with meropenem achieved 100% survival, accompanied by reduced bacterial burden and systemic inflammatory cytokines, consistent with combined antibacterial and host-directed effects, supporting a multifunctional adjuvant profile. This study did not measure bacterial membrane potential in vivo, and the causal role of hyperpolarization in protection or attenuated MIC escalation remains to be determined. - Source: PubMed
Publication date: 2026/04/30
Yeh Jih-ChaoHazam Prakash KishoreLin You-YingChang Yuan-ChihSelvaraj Sanjay PrasadLi Chao-ChinLin Po-YenHuang Yi-PingChang Chi-FonYou Ming-FengChen Jyh-Yih - Host survival during sepsis depends not only on pathogen burden but also on inflammatory thresholds calibrated by the gut microbiota. Here, we show that different survival outcomes were observed in genetically equivalent female C57BL/6 mouse populations depending on their specific gut microbiota configuration. A Muribaculaceae-enriched gut microbiota, characterized by the dominance of Sangeribacter muris KT1-3, predisposed mice to fatal sepsis caused by Acinetobacter baumannii via TLR4-dependent hyperinflammation. This lethal phenotype, reproduced by colonization with S. muris strain KT1-3, was transferable by fecal microbiota transplantation and co-housing. Notably, fixed-dose LPS challenge and ex vivo stimulation assays demonstrated that this configuration induces a heightened TLR4-dependent inflammatory responsiveness independent of bacterial replication. Single-cell transcriptomics revealed that these microbiota-derived factors establish a transcriptionally pre-activated macrophage state, resulting in production of excessive pro-inflammatory cytokines upon challenge. Mechanistically, S. muris strain KT1-3 releases heat-stable and low-molecular-weight (<3 kDa) metabolites that are sufficient to potentiate systemic cytokine surges under a fixed-dose endotoxin challenge in vivo, effectively lowering the host's activation threshold for TLR4-driven signaling. Tlr4-deficient mice harboring the KT1-3-enriched susceptible microbiota survived despite persistent bacterial dissemination, demonstrating that the microbiota-TLR4 axis dictates hyperinflammatory A. baumannii-induced sepsis outcomes by modulating inflammatory magnitude rather than pathogen clearance. Our results provide a conceptual framework for how specific gut microbiota configurations modulate host susceptibility and drive infection resilience. - Source: PubMed
Publication date: 2026/04/30
Jang SeonghanKim Yu-JeongPark JisunKim DajeongKim Tae-HwanLee SoohyunKim Doo-JinRyu Choong-MinSeo Hwi Won - Myocardial ischemia-reperfusion injury (MIRI) remains a critical clinical condition with limited preventive and therapeutic strategies, underscoring the need for novel interventions. The gut-heart axis and exosomal crosstalk hold therapeutic promise for cardioprotection, yet the fundamental question of which specific gut cells release the beneficial exosomes is unanswered. This study aimed to elucidate whether ginseng polysaccharides WGPA exert remote cardiac protection by regulating intestinal immune homeostasis, specifically through promoting the release of exosomes from regulatory T cells (Tregs). Using integrated in vivo and in vitro models, we evaluated the protective effects of WGPA against MIRI. The results demonstrated that WGPA pretreatment significantly attenuated myocardial injury and improved cardiac function. Mechanistically, WGPA selectively activated intestinal Tregs and enhanced the release of HSP70-enriched exosomes. These exosomes entered systemic circulation and were delivered to the heart, where surface HSP70 interacted with TLR4 on cardiomyocytes, activating downstream protective signaling pathways and ultimately suppressing cardiomyocyte death and inflammatory responses. Our study reveals for the first time a complete mechanism by which medicinal plant polysaccharides confer cross-organ cardioprotection via the "intestinal Tregs-exosome-heart" axis, providing a novel theoretical basis and a potential intervention strategy for the prevention and treatment of MIRI. - Source: PubMed
Publication date: 2026/04/28
Li Yuan-YuanSun LinWang YanYang Hua-YiXu De-ShengZhong Yan-ZhuZhang Juan-HongLi YangPi Fang-CaoLi Qi-LuLi Zi-RuiWang Wei-TingChen Ming-TaiLiu Meng-NanSun Qi-diPeng Ming-MingLeung Elaine Lai-HanWu Qi-BiaoHan Ya-LingLiu LiangXie YingZhou Yi-FaZhou Hua - Biomass burning is a major source of fine particulate matter (PM), that can induce oxidative stress and inflammation in the respiratory system, yet its molecular effects remain insufficiently understood. This study investigated the toxicological mechanisms of organic PM extracts from sugarcane burning (SB), forest burning (FB), and cashew nut roasting (CNR) using A549 epithelial monoculture and A549/differentiated THP-1 macrophage-like co-culture models. All extracts induced mitochondrial reactive oxygen species (ROS) in both models, although CNR caused a 15-fold higher response in monoculture. Inflammatory gene expression and secretion of IL-1β, IL-8, and TNF-α were generally stronger in the co-culture, reaching ≥ 10-fold compared with controls, as observed for IL-8 after SB exposure. The enhanced inflammatory response in co-culture was accompanied by increased NF-κB activation and nuclear translocation, which were detected in A549 cells only in the presence of macrophages, underscoring the importance of cell-cell interactions in amplifying PM-induced inflammation. Source-specific chemical composition, particularly differences in oxygenated polycyclic aromatic compounds, was consistent with the distinct oxidative and inflammatory phenotypes observed across extracts. Inhibition of toll-like receptor 4 (TLR4) attenuated NF-κB activation in A549 cells within co-culture, indicating a key role for macrophage-epithelial inflammatory signaling. These findings show that the organic fraction of biomass-derived PM induces source-dependent oxidative and inflammatory responses and identify epithelial-macrophage crosstalk as an important mechanism amplifying inflammatory signaling. The results also support the value of co-culture models for mechanistic hazard identification of biomass-burning emissions. - Source: PubMed
Publication date: 2026/04/29
Frias Daniela PerroniFilho Gildácio Pereira ChavesMoreira Susana Margarida GomesBatistuzzo de Medeiros Silvia ReginaDreij Kristiande Oliveira Galvão Marcos Felipe