Department of Pathogen Biology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, PR China.
Department of Infectious Disease, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, PR China.
J Med Microbiol. 2021 Apr;70(4). doi: 10.1099/jmm.0.001352.
Macrophages polarization is essential in infection control. Llipopolysaccharide (LPS) plays an essential role in host innate immune system-pathogen interaction. The LPS structure of modifies in the adaptation of this pathogen to biofilm-related chronic infection. There have been several studies on LPS induced polarization of human and mouse macrophages with different results. And it was reported that the lipid A structure of the LPS derived from biofilm-forming strain PAO1 was modified. This study aimed to investigate the effect and the involved pathway of LPS from biofilm-forming PAO1 on human and murine macrophage polarization. LPS was isolated from biofilm-forming and planktonic PAO1 and quantified. Then the LPS was added to PMA-differentiated human macrophage THP-1 cells and Raw264.7 murine macrophage cells. The expression of iNOS, Arg-1, , TNF-α, , and was analysed in the different cell lines. The expression of TICAM-1 and MyD88 in human THP-1 macrophages was quantified by Western blot. PAO1 infected macrophages at different polarization states, and the intracellular bacterial growth in macrophages was evaluated. LPS from biofilm-forming PAO1 induced more marked hyperinflammatory responses in THP-1 and Raw264.7 macrophages than LPS derived from planktonic PAO1, and these responses were related to the up-regulation of MyD88. Intracellular growth of PAO1 was significantly increased in THP-1 macrophages polarized by LPS from biofilm-forming PAO1, but decreased both in THP-1 and Raw264.7 macrophages polarized by LPS from planktonic PAO1. The presented study indicates that LPS derived from biofilm-forming PAO1 induces enhanced M1 polarization in human and murine macrophage cell lines than LPS from planktonic PAO1.
巨噬细胞极化在感染控制中至关重要。脂多糖 (LPS) 在宿主先天免疫系统-病原体相互作用中起着重要作用。这种病原体对生物膜相关慢性感染的适应会改变 LPS 的结构。已经有几项关于 LPS 诱导人源和鼠源巨噬细胞极化的研究，但结果并不一致。据报道，生物膜形成的 PAO1 菌株 LPS 的脂质 A 结构发生了修饰。本研究旨在探讨生物膜形成的 PAO1 来源 LPS 对人源和鼠源巨噬细胞极化的影响及其涉及的途径。从生物膜形成和浮游 PAO1 中分离 LPS 并进行定量。然后将 LPS 添加到 PMA 分化的人巨噬细胞 THP-1 细胞和 Raw264.7 鼠源巨噬细胞中。在不同的细胞系中分析 iNOS、Arg-1、TNF-α 和 的表达。通过 Western blot 定量分析人源 THP-1 巨噬细胞中 TICAM-1 和 MyD88 的表达。在不同极化状态下感染巨噬细胞，并评估巨噬细胞内的细菌生长情况。生物膜形成的 PAO1 来源的 LPS 诱导 THP-1 和 Raw264.7 巨噬细胞产生更明显的过度炎症反应，比浮游 PAO1 来源的 LPS 更为显著，这些反应与 MyD88 的上调有关。生物膜形成的 PAO1 来源 LPS 极化的 THP-1 巨噬细胞中 PAO1 的胞内生长明显增加，但浮游 PAO1 来源 LPS 极化的 THP-1 和 Raw264.7 巨噬细胞中 PAO1 的胞内生长均减少。本研究表明，生物膜形成的 PAO1 来源 LPS 诱导人源和鼠源巨噬细胞系中 M1 极化的作用强于浮游 PAO1 来源 LPS。
