Lipopolysaccharide (LPS) produced by P. gingivalis has been reported as a major factor of periodontitis. Recently, LPS has been found to cause neuroinflammation, leading to neurodegeneration such as Alzheimer's disease. Neuroinflammation has also been shown to be involved in developmental disorders, but there are few reports on the relationships between LPS and developmental disorders. On the other hand, we have been shown that the repeated stress such as maternal separation causes behavioral abnormalities like developmental disorders via K^＋-Cl^- co-transporter 2 (KCC2) downregulation in mouse models. Therefore, we hypothesized that LPS causes neuroinflammation and decreases KCC2 that leads to developmental disorders. So, we analyzed KCC2 expression after LPS treatment using primary rat cerebral cortex cells and PC-12 cells. As a result, LPS treatment (10µg/ml) decreased KCC2 expression both in primary rat cerebral cortex cells and PC-12 cells. Gene expression of toll-like receptor4 (TLR4; LPS ligand), IL1-β (inflammation marker), and REST (KCC2 repressor) were up-regulated in PC-12 cells. Moreover, the expression of pWNK, which negatively regulates KCC2, was up-regulated by LPS treatment. These results indicate that we may propose the developmental disorder drug candidates by inhibiting this pathway in the brain.