Department of Laboratory Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Department of Urology, North Kuanren General Hospital, Chongqing, China.
Mediators Inflamm. 2021 May 18;2021:5596339. doi: 10.1155/2021/5596339. eCollection 2021.
Basil polysaccharide (BPS) represents a main active ingredient extracted from basil (Ocimum basilicum L.), which can regulate secondary bacterial pneumonia development in the process of sepsis-mediated immunosuppression.
In this study, a dual model of sepsis-induced secondary pneumonia with cecal ligation and puncture and intratracheal instillation of or was constructed.
The results indicated that BPS-treated mice undergoing CLP showed resistance to secondary pneumonia. Compared with the IgG-treated group, BPS-treated mice exhibited better survival rate along with a higher bacterial clearance rate. Additionally, BPS treatment attenuated cell apoptosis, enhanced lymphocyte and macrophage recruitment to the lung, promoted pulmonary cytokine production, and significantly enhanced CC receptor ligand 4 (CCL4). Notably, recombinant CCL4 protein could enhance the protective effect on -induced secondary pulmonary infection of septic mice, which indicated that BPS-induced CCL4 partially mediated resistance to secondary bacterial pneumonia. In addition, BPS priming markedly promoted the phagocytosis of alveolar macrophages while killing , which was related to the enhanced p38MAPK signal transduction pathway activation. Moreover, BPS also played a protective role in sepsis-induced secondary pneumonia by inducing Treg cell differentiation.
Collectively, these results shed novel lights on the BPS treatment mechanism in sepsis-induced secondary pneumonia in mice.
罗勒多糖(BPS)是从罗勒(Ocimum basilicum L.)中提取的主要活性成分,可调节脓毒症介导的免疫抑制过程中继发性细菌性肺炎的发展。
本研究构建了盲肠结扎和穿刺联合气管内滴注 或 的脓毒症诱导的继发性肺炎双重模型。
结果表明,接受 CLP 的 BPS 处理的小鼠对继发性 肺炎具有抵抗力。与 IgG 处理组相比,BPS 处理组的小鼠具有更高的生存率和更高的细菌清除率。此外,BPS 治疗可减轻细胞凋亡,增强淋巴细胞和巨噬细胞向肺部募集,促进肺部细胞因子产生,并显著增强 C 型凝集素受体 4(CCL4)。值得注意的是,重组 CCL4 蛋白可增强对脓毒症小鼠 诱导的继发性肺部感染的保护作用,表明 BPS 诱导的 CCL4 部分介导了对继发性细菌性肺炎的抵抗力。此外,BPS 预刺激明显促进肺泡巨噬细胞吞噬 ,并杀死 ,这与增强的 p38MAPK 信号转导途径的激活有关。此外,BPS 通过诱导 Treg 细胞分化在脓毒症诱导的继发性 肺炎中也发挥了保护作用。
综上所述,这些结果为 BPS 治疗脓毒症诱导的继发性 肺炎的机制提供了新的见解。