Lipopolysaccharide Preconditioning Induces an Anti-inflammatory Phenotype in BV2 Microglia

Increasing evidence indicates that endotoxin tolerance is an essential immune-homeostatic response to repeated exposure to lipopolysaccharide (LPS) that induces a state of altered responsiveness in macrophage, resulting in repression of pro-inflammatory gene expression and increased expression of factors that mediate the resolution of inflammation. In this study, quantitative real-time polymerase chain reaction and Western blot for M1 and M2 markers were performed to characterize phenotypic changes of BV2 microglia. We found that the cytokine and chemokine expression during endotoxin tolerance were mostly similar to those found during M2 polarization. We further examined the expression of M1 and M2 markers in CD11b⁺ BV2 by double immunofluorescent staining. The expression of M2 markers (CD206) increased, whereas the expression of M1 (CD54) markers reduced during endotoxin tolerance. Moreover, expression of different transcription factor, known for their function in the regulation of pro- and anti-inflammatory reaction, was also different. Our data demonstrate that repeat LPS treatment activates a differentiation program that leads to microglial polarization toward M2-like phenotype.