Ask about this productRelated genes to: TLR4 Blocking Peptide
- 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 Blocking Peptide
Related articles to: TLR4 Blocking Peptide
- Pseudomonas (P.) aeruginosa is an opportunistic pathogen closely linked to Cystic Fibrosis (CF). Recent publications emphasize that an accumulation of bacterial derived extracellular vesicles within the circulation might be associated with the pathogenesis of various chronic inflammatory diseases and could potentially be used as diagnostic tool. - Source: PubMed
Publication date: 2026/08/13
von Mauch CelinaEdrich Lisa-MariaSobel JuliaGeppert AnnikaMattner JochenArnold PhilippHoerning AndréGuenther ClaudiaSchnell AlexanderStolzer Iris - Acute coliform mastitis (ACM) is an inflammatory disease of the mammary gland and may be accompanied by fatal systemic manifestations. The impact of virulence factors of coliform pathotypes on ACM severity remains unclear. The current work investigated the molecular events by which pathogens' virulence broadens local mammary infection to metabolic disturbances and systemic outcomes. A total of 168 Holstein cows with ACM were investigated; 18 met the inclusion criteria and were categorized into localized ACM (LACM, n = 9) and systemic ACM (SACM, n = 9) based on udder inflammation severity, clinical manifestations, and SCC, along with 10 healthy controls. Coliform bacteria (Escherichia coli and Klebsiella pneumoniae) were identified by MALDI-TOF MS, serotyped by O/H/K agglutination, screened for antimicrobial susceptibility, and virulence determinants by PCR. Tested SACM strains exhibited XDR phenotypes with high MAR indices. They harbored multiple virulence determinants (iss, ompT, iucD), whereas LACM strains carried only iss and were associated with localized inflammatory reactions. Antimicrobial peptides, acute-phase proteins, markers of hepatobiliary/renal and cardiac injury, metabolic imbalance, and TLR4/CD-14/LRRK-1-mediated inflammatory signaling and suppression of antioxidant defense were more intensified in SACM than in LACM and controls. The correlation matrix and Mantel test revealed significant integration of virulence-induced systemic host responses in the SACM group, evidenced by strong inter-organ biomarker associations and coordinated oxidative-inflammatory cascade networks (r>0.75, P≤ 0.01). Composite host response modeling supported that virulence traits are linked to mastitis severity. Thus, combining virulence profiling with host-response biomarkers offers an approach to forecasting mastitis progression toward systemic oxidative metabolic dysregulation and to improving clinical management. - Source: PubMed
Publication date: 2026/08/13
El-Sebaey Ahmed MSelim Ahmed MagdyAbramov Pavel NAteya AhmedKiskó GabriellaBelák ÁgnesElzhraa FatmaRagab Wafaa - Sterile inflammation driven by cell-free DNA (cfDNA) and reactive oxygen species (ROS) underlies acute inflammatory disorders, yet current therapies fail to specifically target these upstream mediators. We report a dynamic covalent/coordinated nanonetwork (DC NNW) that combines drug delivery, DNase-mimetic and ROS-scavenging functions through reaction-induced self-assembly and cerium coordination. DC NNWs efficiently degrade cfDNA, scavenge ROS, and release the loaded therapeutics, suppressing TLR9/NF-κB/NLRP3 and TLR4/MyD88/JAK signaling. In murine models of acute kidney injury (AKI) and endometritis, DC NNWs selectively accumulated in inflamed tissues, restored organ function, alleviated injury, and reduced oxidative stress. Transcriptomic analysis further showed downregulation of pro-inflammatory and neutrophil extracellular trap (NET)-associated genes, alongside activation of metabolic repair pathways including fatty acid oxidation and mitochondrial respiration. This multifunctional nanozyme platform, with its drug delivery properties, offers a targeted and upstream approach for modulating innate immune activation and metabolic dysfunction in AKI, endometritis, and other sterile inflammatory diseases. - Source: PubMed
Publication date: 2026/08/13
Huang Yan-QiangZhang XiaoLi WenluWu YiWu HaoyueJin AolinLiu ZuohaoQiu ShaocaiLi DongLi XiaomeiWei ZhonghengJiang WenxiaoLiu YongShi YangLi Yuanfeng - Immunosenescence increases susceptibility to varicella-zoster virus (VZV) infection in the elderly while compromising vaccine responsiveness. Although clinical adjuvants such as AS01 have improved vaccine efficacy, challenges associated with saponin-based components and separate antigen-adjuvant formulations persist. Here, we developed a nanovaccine, NP(gEIM), that co-encapsulates VZV glycoprotein E (gE) with the TLR4 agonist MPLA and TLR7/8 agonist IMQ in lipid nanoparticles via flash nanocomplexation (FNC), enabling coordinated co-delivery of antigen and adjuvants. NP(gEIM) efficiently targeted draining lymph nodes and promoted antigen-presenting cell uptake and maturation. In young and aged mice, NP(gEIM) elicited gE-specific antibody responses and Th1-biased cellular immunity comparable to AS01-adjuvanted gE vaccines while exceeding aluminum-adjuvanted vaccines. Moreover, NP(gEIM) enhanced IFN-γ and TNF-α production by antigen-specific CD4 and CD8 T cells while reducing immunosuppressive Treg and MDSC populations in aged mice. Notably, NP(gEIM) reshaped the TCR repertoire by promoting selective expansion of putative antigen-responsive T cell clones and altering TCR V/J gene usage and CDR3 length distribution, providing molecular insights into vaccine-induced T cell responses. Collectively, this study presents a nanovaccine strategy enabling coordinated delivery of antigen and dual TLR agonists. By integrating humoral and cellular immunity with TCR repertoire modulation, NP(gEIM) offers a potential strategy for improving vaccine responses in aging populations and developing vaccines against age-associated infectious diseases. - Source: PubMed
Publication date: 2026/08/13
Chen HaolinZhang ZhihuiWen ZhenfuYang ZeyuLi LiyanWang ShengGao QiangLiu HongLiu LixinChen Yongming - Myopia progression is closely associated with scleral remodeling, in which oxidative stress, inflammation, and disruption of extracellular matrix (ECM) homeostasis may play important roles. Betaine has antioxidant and anti-inflammatory properties, but its effects on myopic scleral remodeling remain unclear. Public transcriptomic data, network pharmacology, and molecular docking were used as exploratory approaches to identify potentially relevant molecules and pathways. The in vivo and in vitro effects of betaine were subsequently evaluated in lens-induced myopia (LIM) guinea pigs and in lipopolysaccharide (LPS)-stimulated primary guinea pig scleral fibroblasts, respectively. As a result, LIM induced axial elongation, a myopic refractive shift, scleral structural alterations, reactive oxygen species (ROS) accumulation, inflammation, and disruption of ECM homeostasis. These changes were accompanied by activation of the toll-like receptor 4 (TLR4)/transforming growth factor-β-activated kinase 1 (TAK1)/nuclear factor-κB (NF-κB) pathway and increased tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) levels. Betaine attenuated these changes, reduced matrix metalloproteinase-2 (MMP2) expression, and partially restored tissue inhibitor of metalloproteinases-2 (TIMP2), Collagen I, and α-smooth muscle actin (α-SMA) levels. In vitro, betaine partially restored cell viability, reduced ROS and inflammatory cytokine levels, suppressed TLR4/TAK1/NF-κB pathway activation, and ameliorated alterations in ECM-related proteins. Exploratory computational analyses suggested possible associations with inflammation-, oxidative stress-, and ECM-related pathways. Collectively, betaine attenuated LIM-induced myopia progression and scleral remodeling, potentially by reducing oxidative stress and inflammation, suppressing TLR4/TAK1/NF-κB signaling, and improving ECM homeostasis. - Source: PubMed
Publication date: 2026/08/13
Zhang YinqiaoXie YunxiaoYang ZhaohuiGao RunzeYu ShuwenHao JiawenMa ZhongyuYang YuantingZhang RuixueBi HongshengGuo Dadong