Ask about this productRelated genes to: TLR4 antibody
- 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 antibody
Related articles to: TLR4 antibody
- Biogenesis of lysosome-related organelles complex 1 subunit 1 (BLOC1S1, also known as BLOS1) is a key gene involved in phagosome-lysosome maturation, transport, and autophagosome fusion, and it plays a crucial role in host resistance to Brucella infection. This study aimed to examine the effects of BLOS1 overexpression (oeBLOS1) on the stress response of goat macrophages and on intestinal microbiota composition. Peripheral blood mononuclear cells (PBMCs) were isolated from oeBLOS1 and wild-type (WT) goats and differentiated into macrophages. These macrophages were then stimulated with Brucella LPS to assess cytokine secretion and autophagy levels. Metagenomic sequencing was also performed to analyze the structural and functional profiles of the rectal fecal microbiota in these goats. After Brucella LPS stimulation, oeBLOS1 goat macrophages rapidly activated the NF-κB and TLR4 signaling pathways, promoting the synthesis and secretion of cytokines such as TNF-α (P < 0.05). Brucella LPS challenge also significantly increased the transcription of autophagy-related genes such as LAMP2 and BECN1, enhancing autophagic activity and bacterial clearance (P < 0.05). Furthermore, oeBLOS1 altered the intestinal microbiota, significantly enriching pathways linked to membrane transport and cell motility, and reducing the abundance of virulence factors and opportunistic pathogens, which may contribute to intestinal immune homeostasis. In summary, oeBLOS1 may help counteract Brucella LPS-induced infection by promoting the immune response, enhancing autophagy. In addition, it is associated with remodeling gut microbial function, suggesting a potential role in disease resistance. - Source: PubMed
Publication date: 2026/05/19
Wang CongliangLiu XiaoyuWan ShichengXie FangdeDai JianqiChen WenboQu LeiZhang LeiLi NaDu XiaominZhu HaijingHua Jinlian - Guanxin Ⅱ (GXⅡ) is a traditional Chinese herbal formula, which has the functions of activating blood to resolve stasis and move qi to relieve pain. Qi and blood stagnant is regarded as the main pathogenesis of atherosclerosis (AS) and depression, but the specific mechanism of GXⅡ in the treatment of AS comorbid depression (co-depression) remains unclear. - Source: PubMed
Publication date: 2026/05/19
Luo QiangLiu XuZhao YulongFan YuzhenLin YemingWu XiaoyunWen YouliangZeng XinhuaZhou Junjie - Annexin A1 (AnxA1) is a key anti-inflammatory mediator that regulates both innate and adaptive immunity, promoting resolution of inflammation and tissue repair. It is highly expressed in neutrophils, macrophages, dendritic cells, and select lymphocyte subsets, where it limits excessive immune activation and maintains immune homeostasis. Through binding to the G protein-coupled receptor formyl peptide receptor 2 (FPR2/ALX), AnxA1 induces neutrophil apoptosis and promotes macrophage polarization toward an anti-inflammatory M2 phenotype. In adaptive immunity, AnxA1 regulates CD4 T-cell differentiation in a lineage-specific manner, promoting Th1 and Th17 responses while suppressing Th2 polarization; its deficiency skews T cells toward a Th2 phenotype with increased IL-4/IL-13 and reduced IL-17, highlighting its role in maintaining T-cell balance. In autoimmune and inflammatory disorders such as rheumatoid arthritis, lupus, type-1 diabetes, and multiple sclerosis, hyperactivation of toll-like receptor-4 (TLR4) and epidermal growth factor receptor (EGFR) drives STAT1-dependent signaling, sustaining cytokine production and tissue injury. The Annexin A2 (AnxA2)-EGFR complex further amplifies this response by downregulating AnxA1 and reinforcing pro-inflammatory signaling pathways. In contrast, AnxA1 engagement with EGFR and FPR2 redirects signaling toward STAT3, enhancing IL-10 and TGF-β production while suppressing STAT1-driven pathways. This STAT1-STAT3 balance is critical for immune resolution, inflammation control, and tissue homeostasis. Therapeutically, AnxA1-based strategies suppress STAT1 signaling and promote a regulated STAT3/SOCS3 axis associated with immune resolution, while limiting pathogenic Th17-associated STAT3 activity. Overall, AnxA1 acts as a molecular switch integrating receptor-mediated signals to fine-tune immune responses and mitigate tissue damage in chronic inflammatory and autoimmune diseases. - Source: PubMed
Publication date: 2026/05/19
Ambrish ThrupthiJayaswamy Pavan KHaridas VikramKellarai AdithiShetty SukanyaSheety Praveenkumar - This study investigated the effect of xylanase supplementation on growth performance and intestinal barrier integrity in pigs fed low metabolizable energy (ME) diets. Eighteen growing pigs (41.2 ± 0.8 kg) were allocated to three diets in a complete randomized design, including: basal diet (3300 kcal ME/kg), low ME diet (3200 kcal/kg), and low ME supplemented with 0.01% xylanase enzyme. After 14 days, performance and intestinal mucosa parameters, including the expression of molecules related to physiology and mucosal immunity, were assessed using a one-way ANOVA, followed by Tukey's test. Pigs fed the xylanase-supplemented diet had higher (P < 0.05) final bodyweight (55.45 kg) than low ME (51.10 kg), and comparable to basal (55.24 kg). Feed conversion ratio and feed costs were also improved (P < 0.05) in the xylanase group (2.19; 43.6 baht/kg) compared with both low ME (2.69; 52.2 baht/kg) and basal diet (2.46; 46.3 baht/kg). Xylanase supplementation upregulated (P < 0.05) ileal glucose transporters (SGLT1 and GLUT2), colonic immune-related genes (TLR4, BD, BD3 and BD4), compared to the other groups. Tight junction genes (CLDN2, CLDN5, and ZO1) were upregulated (P < 0.05) in the colon of xylanase-fed pigs compared to the low ME. Xylanase also upregulated (P < 0.05) mucosal defense factors (sIgA components and mucin 2) compared with the control. In conclusion, xylanase supplementation restored growth performance to the basal level while enhancing feed efficiency and intestinal barrier integrity in pigs fed low-ME diets. - Source: PubMed
Publication date: 2026/05/18
Lothong MuttarinRukarcheep DranSamritwatchasai TheerawatPoonyachoti SutthasineeKaewtapee Chanwit - Chaihu Guizhi Ganjiang Decoction (CGGD) is a clinically proven prescription effective against metabolic dysfunction-associated steatohepatitis (MASH). However, its chemical constituents with the lipid-lowering and anti-inflammatory bioactivities and underlying mechanisms remain unclear. This study aimed to characterize the chemical profile of CGGD while elucidating their lipolytic and anti-inflammatory activities and mechanisms. Using UHPLC-Q-TOF-MS/MS, 209 compounds were identified in CGGD, categorized into 52 saponins, 103 flavonoids, 17 gingerols, 21 organic acids, and 16 others, with 13 putative unvalidated new compounds. Nineteen prototype components were detected in hepatic tissues, with saikosaponin A, baicalin, wogonoside, skullcapflavone II, and glycyrrhizin exhibiting strong binding affinities toward PPARα and TLR4 proteins. These components significantly reduced triglyceride (TG) accumulation in FFA-induced HepG2 steatosis cells, confirmed by oil red O staining and TG quantification. Mechanistically, saikosaponin A and baicalin upregulated PPARα and its downstream genes (CPT1A, FABP1, ACOX1) to promote fatty acid transport and oxidation. Meanwhile, saikosaponin A, baicalin, and wogonoside significantly suppressed mRNA expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) in LPS-stimulated RAW264.7 macrophages, and saikosaponin A and wogonoside further inhibited the expression of TLR4, MyD88, and phosphorylated NFκB, thereby attenuating inflammation. In conclusion, this study established a comprehensive methodology for profiling the chemical constituents of CGGD and identified saikosaponin A, baicalin, wogonoside, skullcapflavone II, and glycyrrhizin as its key anti-MASH components. Their lipid-lowering and anti-inflammatory activities were mediated through the PPARα-regulated fatty acid metabolism pathway and the TLR4/MyD88/NFκB signaling pathway, respectively, offering a scientific basis for the clinical application of CGGD in MASH. - Source: PubMed
Publication date: 2026/05/18
Wu HaoWang TengtengCai ShengnanQiao YunLiu JieLi YuetingXiao Hongbin