Luo Fengling, Sun Xiaoming, Qu Zhen, Zhang Xiaolian
State Key Laboratory of Virology, Medical Research Institute of Wuhan University and Department of Immunology and Hubei Province Key Laboratory of Allergy and Immunology, Wuhan University School of Medicine, Donghu Road 185#, Wuhan, 430071, Hubei Province, China.
World J Microbiol Biotechnol. 2016 Feb;32(2):22. doi: 10.1007/s11274-015-1978-z. Epub 2016 Jan 8.
Recently, macrophages were shown to be capable of differentiating toward two phenotypes after antigen stimulation: a classically activated (M1) or an alternatively activated phenotype (M2). To investigate the effect of Salmonella enteric serovar typhimurium (S. typhimurium) on macrophage differentiation, we compared macrophage phenotypes after infection of murine bone marrow-derived macrophages with wild-type S. typhimurium and its isogenic rfc mutant. S. typhimurium C5 induced M1 macrophage polarization and enhanced inducible nitric oxide synthase expression by macrophages; this induction was dependent on Toll-like receptor 4. In contrast, the Δrfc mutant (S. typhimurium C5 rfc::Km(r)) lost this function and induced an M2 response in the macrophages. Here, we propose that S. typhimurium C5 is capable of polarizing macrophages towards the M1 phenotype and that this polarization is dependent on the O antigen encoded by rfc. Our finding indicates that M1 macrophage polarization induced by S. typhimurium may be related to the ability of this intracellular bacterium to survive and replicate within macrophages, which is essential for systemic disease.
最近研究表明，巨噬细胞在抗原刺激后能够分化为两种表型：经典活化型（M1）或替代活化型（M2）。为了研究鼠伤寒沙门氏菌（S. typhimurium）对巨噬细胞分化的影响，我们比较了野生型鼠伤寒沙门氏菌及其同基因rfc突变体感染小鼠骨髓来源的巨噬细胞后的巨噬细胞表型。鼠伤寒沙门氏菌C5诱导M1巨噬细胞极化，并增强巨噬细胞中诱导型一氧化氮合酶的表达；这种诱导依赖于Toll样受体4。相反，Δrfc突变体（鼠伤寒沙门氏菌C5 rfc::Km(r)）失去了该功能，并在巨噬细胞中诱导了M2反应。在此，我们提出鼠伤寒沙门氏菌C5能够使巨噬细胞向M1表型极化，并且这种极化依赖于rfc编码的O抗原。我们的研究结果表明，鼠伤寒沙门氏菌诱导的M1巨噬细胞极化可能与其在巨噬细胞内存活和复制的能力有关，这对于全身性疾病至关重要。
