LQVTDSGLYRCVIYHPP is a myeloid cell triggered receptor 1 (TREM-1) inhibitory peptide [1]. LQVTDSGLYRCVIYHPP inhibits downstream inflammatory signaling pathways by competitively binding to TREM-1 and blocking its activation, thereby exerting anti-inflammatory effects [2]. LQVTDSGLYRCVIYHPP can be used in the study of infectious diseases, inflammatory diseases and tumor immunoregulation [3].
In macrophages, treatment with LQVTDSGLYRCVIYHPP (50μM; 24h) significantly reduced the relative levels of LPS-stimulated IL-6, TNFα, CD14 and TREM-1 mRNA transcripts [4]. In microglial, LQVTDSGLYRCVIYHPP (10μM; 24h) substantially decreased mRNA levels of proinflammatory cytokines (NLRP3, IL-1β, IL-18, IL-6, CD16, CD32, and iNOS) and chemokines (MCP-1, CXCL-1, and CXCL-2) [5]. In human corneal epithelial cells, LQVTDSGLYRCVIYHPP (50μM; 24h) induced TREM-1 blockage significantly inhibited the production of TNF-α, IL-1β, IL-6, and IL-8 upon A. fumigatus infection THCEs [6].
In mice cerebral ischemia/reperfusion (I/R) model, after pharmacologic inhibition of TREM-1 with synthetic peptide LQVTDSGLYRCVIYHPP (1mg/kg; intranasal administration; 3d), ischemia-induced infarction and neuronal injury were substantially alleviated [5]. Cecal ligation and puncture (CLP)-induced sepsis rat model, LQVTDSGLYRCVIYHPP (3.5mg/kg; iv; single injection) inhibits the elevation of proinflammatory cytokines TNF-α, IL-6, and IL-1β, thereby alleviating systemic and distant inflammatory responses [7]. In subarachnoid hemorrhage model, TREM-1 inhibition with LQVTDSGLYRCVIYHPP (1mg/kg; intranasal administration; 24h) improved neurological deficits, mitigated brain water content, and preserved brain-blood barrier integrity 24h after SAH [8].
References:
[1]. Siskind S, Brenner M, Wang P. TREM-1 modulation strategies for sepsis. Frontiers in Immunology. 2022 Jun 15; 13: 907387.
[2]. Fu L, Han L, Xie C, et al. Identification of extracellular actin as a ligand for triggering receptor expressed on myeloid cells-1 signaling. Frontiers in immunology. 2017 Aug 7; 8: 917.
[3]. Theobald V, Schmitt FC, Middel CS, et al. Triggering receptor expressed on myeloid cells-1 in sepsis, and current insights into clinical studies. Critical Care. 2024 Jan 9; 28(1): 17.
[4]. Liu M, Zhang Y, Xiong JY, et al. Etomidate Mitigates Lipopolysaccharide-Induced CD14 and TREM-1 Expression, NF-κB Activation, and Pro-inflammatory Cytokine Production in Rat Macrophages. Inflammation. 2016 Feb; 39(1): 327-335.
[5]. Xu P, Zhang X, Liu Q, et al. Microglial TREM-1 receptor mediates neuroinflammatory injury via interaction with SYK in experimental ischemic stroke. Cell death & disease. 2019 Jul 19; 10(8): 555.
[6]. Hu LT, Du ZD, Zhao GQ, et al. Role of TREM-1 in response to Aspergillus fumigatus infection in corneal epithelial cells. International Immunopharmacology. 2014 Nov 1; 23(1): 288-293.
[7]. Shi X, Zhang Y, Wang H, et al. Effect of triggering receptor expressed on myeloid cells 1 (TREM-1) blockade in rats with cecal ligation and puncture (CLP)-induced sepsis. Medical Science Monitor: International Medical Journal of Experimental and Clinical Research. 2017 Oct 23; 23: 5049.
[8]. Xu P, Hong Y, Xie Y, et al. TREM-1 exacerbates neuroinflammatory injury via NLRP3 inflammasome-mediated pyroptosis in experimental subarachnoid hemorrhage. Translational Stroke Research. 2021 Aug; 12: 643-659.
LQVTDSGLYRCVIYHPP是一种髓系细胞触发受体1（TREM-1）抑制肽 [1]。LQVTDSGLYRCVIYHPP 通过竞争性结合TREM-1并阻断其活化来抑制下游炎症信号通路，从而发挥抗炎作用 [2]。LQVTDSGLYRCVIYHPP可用于研究传染病、炎症性疾病和肿瘤免疫调节 [3]。
在巨噬细胞中，LQVTDSGLYRCVIYHPP（50μM；24h）处理可显著降低LPS刺激的IL-6、TNFα、CD14和TREM-1 mRNA转录物的相对水平 [4]。在小胶质细胞中，LQVTDSGLYRCVIYHPP（10μM；24h）显著降低了促炎细胞因子（NLRP3、IL-1β、IL-18、IL-6、CD16、CD32和iNOS）以及趋化因子（MCP-1、CXCL-1和CXCL-2）的mRNA水平 [5]。在人角膜上皮细胞中，LQVTDSGLYRCVIYHPP（50μM；24h）诱导的TREM-1阻断显著抑制了烟曲霉感染THCE后TNF-α、IL-1β、IL-6和IL-8的产生 [6]。
在小鼠脑缺血/再灌注（I/R）模型中，用合成肽LQVTDSGLYRCVIYHPP（1mg/kg；鼻腔给药；3d）药物抑制TREM-1后，缺血引起的梗死和神经元损伤得到显著减轻 [5]。在盲肠结扎穿刺（CLP）诱发的脓毒症大鼠模型中，LQVTDSGLYRCVIYHPP（3.5mg/kg；iv；单次注射）可抑制促炎细胞因子TNF-α、IL-6和IL-1β的升高，从而减轻全身和远处的炎症反应 [7]。在蛛网膜下腔出血（SAH）模型中，用LQVTDSGLYRCVIYHPP（1mg/kg；鼻内给药；24h）抑制TREM-1可改善神经功能缺损，降低脑含水量，并在SAH后24小时维持脑血屏障完整性 [8]。