Ask about this productRelated genes to: TLR5 Blocking Peptide
- Gene:
- TLR5 NIH gene
- Name:
- toll like receptor 5
- Previous symbol:
- SLEB1
- Synonyms:
- TIL3, FLJ10052, MGC126430, MGC126431
- Chromosome:
- 1q41
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-25
- Date modifiied:
- 2016-10-05
Related products to: TLR5 Blocking Peptide
Related articles to: TLR5 Blocking Peptide
- Infectious hematopoietic necrosis virus (IHNV) is a significant viral pathogen that affects salmonids, leading to high mortality and substantial economic losses in aquaculture. The current vaccine strategies focus on use of DNA and inactivated vaccines. However, these strategies face limitations concerning biosafety and efficacy. Therefore, in this work, we employed an approach based on the immunoinformatic platform to develop a multi-epitope vaccine against IHNV. For that purpose, we analyzed the glycoprotein of IHNV and identified highly antigenic and non-allergenic cytotoxic T lymphocyte (CTL), helper T lymphocyte (HTL), and B-cell epitopes. The different epitopes were assembled with rational linkers, and the N-terminal flagellin FliC adjuvant was added to enhance immunogenicity. The designed vaccine showed favorable physicochemical properties and high structural stability, which was validated through modeling and refinement. Moreover, the molecular docking of the designed vaccine with toll-like receptor 5 (TLR5) and molecular dynamics simulation revealed stable and strong interactions between the vaccine and TLR5, demonstrating that the designed vaccine can activate innate immunity. Furthermore, in silico immune simulations demonstrate a robust humoral and cellular immune response following multiple doses. These findings provide a promising framework for the development of a novel, safe, and effective vaccine against the IHNV infection in Atlantic salmon. - Source: PubMed
Publication date: 2026/05/11
Abdellaoui NajibLim Jae-WoongHan Hyun-JaCho Mi YoungKim Min Sun - Despite the similarities, Crohn's disease (CD) and ulcerative colitis (UC), the two major subtypes of inflammatory bowel disease (IBD), exhibit distinctions. The increasing burden of IBD necessitates discovering novel diagnostic markers. Considering the importance of distinguishing between CD and UC in selecting therapeutic strategies in clinical settings, this investigation focused on identifying subtype-specific blood biomarkers. - Source: PubMed
Publication date: 2026/05/04
Mokaram Doust Delkhah Arman - Host-directed strategies that enhance early innate immune defense are increasingly recognized as important adjunct approaches for controlling mycobacterial infections. Flagellin, a classical ligand of Toll-like receptor 5 (TLR5), has been widely studied as a vaccine adjuvant. However, whether it can transiently modulate innate immunity to enhance host resistance against mycobacterial infection without inducing sustained inflammation remains unclear in vivo. In this study, we systematically evaluated this question using a zebrafish-Mycobacterium marinum infection model. Our results demonstrate that a single exposure to Escherichia coli-derived flagellin significantly reduces bacterial burden and improves host survival upon subsequent infection, without disrupting immune homeostasis. Mechanistically, this protective effect depends on the TLR5-MyD88 signaling pathway and is associated with enhanced early inflammatory responses, as well as accelerated recruitment of neutrophils and macrophages. Notably, even after the resolution of initial inflammation, the host exhibits an enhanced responsiveness to secondary stimulation, resembling features of trained immunity, suggesting that flagellin may act as an inducer of innate immune memory. Collectively, our findings provide in vivo evidence that flagellin enhances early host defense against mycobacterial infection by modulating innate immunity and support the utility of the zebrafish model for evaluating immunomodulator-induced protection. - Source: PubMed
Publication date: 2026/05/01
Dai CongyiZhou JingGuo WenjuanWang HaitaoSun TaoSong ShuWang HaiyingYan Bo - Bacillus velezensis has emerged as a promising probiotic in aquaculture; however, the mechanisms by which it modulates host innate immunity and gut homeostasis in teleost fish remain poorly understood. In this study, interactions among B. velezensis D1, TLR5-associated immune signaling, and gut microbiota dynamics were investigated using an integrated in vitro and in vivo model in Asian swamp eel. In vitro interaction assays demonstrated a selective interaction between eel TLR5 and the flagellar hook protein FlgE, which was validated by co-immunoprecipitation, showing a distinct band at approximately 48 kDa. No interaction was detected with FliC or FliD, and all negative controls were non-reactive, indicating selective association between FlgE and eel TLR5. This interaction suggests a potential link between TLR5-mediated probiotic sensing and downstream immune responses, which may be associated with subsequent intestinal remodeling and gut microbiota restructuring Dietary supplementation altered TLR5, IL-6, IL-1β, and TNF-α expression in spleen, liver, and gut, showing significant early upregulation (6-12 h, p < 0.01) and peak responses at 24-48 h (p < 0.001), with gene- and tissue-specific patterns. Histomorphological analysis revealed significant improvements in gut structure, including increased villus height and width, as well as intestinal wall and muscle layer thickness. Furthermore, 16S rRNA gene sequencing showed that probiotic supplementation significantly altered gut microbial communities. The probiotic group exhibited higher microbial richness, with 527 distinct OTUs compared to 239 in the control group. Beneficial phyla, including Firmicutes and Actinobacteria, increased, while Proteobacteria decreased. These findings suggest that TLR5-associated immune responses may be linked to the observed restructuring of gut microbiota, indicating a coordinated relationship between host immune activation and microbial community modulation following probiotic supplementation. Overall, this study provides insights into host-microbe interactions and supports the potential application of B. velezensis as a probiotic in sustainable aquaculture. - Source: PubMed
Publication date: 2026/04/30
Nassar NourhanKhan Ibrar MuhammadKhan SamiullahQadeer AbdulDu NiWang Zaigui - Avian influenza virus primarily invades the respiratory mucosa, necessitating the establishment of a robust mucosal secretory IgA (sIgA) barrier. However, the efficacy of avian mucosal vaccines is often hindered by inefficient antigen uptake and immune tolerance. Consequently, modern vaccine strategies focus on active targeting delivery, immune microenvironment remodeling, and activation of multifaceted immune responses. The immunogenicity and molecular mechanisms of a novel Salmonella-delivered self-amplifying RNA (saRNA) vector platform were evaluated in this study. This platform integrates bacterial surface display of a dendritic cell (DC)-targeting nanobody (Nb-phage54 via LppOmpA) with co-expression of molecular adjuvants against H9N2 influenza. The expression of HA1 and NA antigens from recombinant plasmids (pYL673, pYL679, and pYL681) was confirmed using confocal microscopy and Western blot analysis. In vitro assays revealed that the Nb-mediated targeting strain (S673) significantly increased invasion efficiency into bone marrow-derived dendritic cells and up-regulated the transcription of CCL5, CCR7, CD83, and CD86, effectively promoting DC maturation. Transcriptomic analysis (RNA-seq) revealed divergent mechanisms among vaccine candidates. The non-targeting group (S615) primarily activated antiviral innate pathways, such as JAK-STAT, whereas the targeting group (S673) significantly improved antigen processing, presentation, and natural killer cell-mediated cytotoxicity. Moreover, the adjuvant-integrated groups, S679 (CpG) and S681 (FliC), specifically triggered Toll-like receptor-21 (TLR21) and TLR5 signaling cascades by increasing cell adhesion, phagocytosis, and transmembrane signal transduction. Animal trials revealed that the targeted adjuvant vectors (S679 and S681) significantly elevated serum IgG and intestinal mucosal sIgA titers in chickens. The S679 group excelled in stimulating lymphocyte proliferation and secreting interferon-gamma and interleukin-4, indicating a potent Th1/Th2 balanced response. Challenge experiments with H9N2 virus confirmed that S679 and S681 effectively mitigated weight loss, shortened the viral shedding window, reduced viral loads in the lungs and trachea, and significantly alleviated respiratory pathological damage and inflammation. The DC-targeting saRNA-Salmonella vector developed in this study, particularly when synergized with CpG or FliC adjuvants, induced robust systemic, mucosal, and cellular immunity by activating specific intracellular signaling cascades. These findings demonstrate that this platform is a highly effective and promising candidate strategy for preventing and controlling H9N2 avian influenza. - Source: PubMed
Publication date: 2026/04/24
Wang MingyueGao YupengZhang YuxiYang TianruiZhang YuhangSun YanGuo QiyuZhang GeruiGong JinshuoWang ZhannanWang ChunfengJiang Yanlong