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Microglia activation plays vital roles in neuroinflammatory pathologys. Lemurs tyrosine kinase 2 (LMTK2) was reported to regulate NF-κB signals. In the present study, the roles of LMTK2 were investigated in lipopolysaccharide (LPS)-treated BV-2 cells. Reverse transcription-quantitative (RT-q)PCR and western blotting (WB) were utilized to analyze LMTK2 levels in LPS-treated BV2 cells. MTT assay determined cell viabilities. Nitric oxide (NO) and prostaglandin E2 (PGE2) levels were assessed through Griess and enzyme-linked immunosorbent assay (ELISA), respectively. The expression level of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) were detected through RT-qPCR and WB. The release of inflammatory mediators under LPS stimulation, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6 and IL-10, were analyzed through ELISA. WB was used to analyze the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1)/NAD(P)H dehydrogenase quinone 1 (NQO1) signal pathway. The results showed that the levels of the inflammatory mediators, iNOS, NO, COX-2 and PGE2, along with pro-inflammatory factors, TNF-α, IL-1β and IL-6, were significantly decreased following the induction of exogenous LMTK2 expression by LMTK2 overexpression plasmids in LPS-induced BV2 microglia. In contrast, anti-inflammatory factor IL-10 showed obvious decrease. Additionally, LMTK2 overexpression induced the elevation of Nrf2 in the cytoplasm and nucleus, along with the upregulation of HO-1 and NQO1 expression. In conclusion, LMTK2 is postulated to regulate neuroinflammation possibly through Nrf2 pathway. The present study is essential to reveal the underlying function of LMTK2 and to identify novel therapeutic targets for drug development in treating neuroinflammation.

Neuromyelitis optica spectrum disorder (NMOSD) is an inflammatory demyelinating disease of the central nervous system. The differential diagnosis of NMOSD in clinical practice is often challenging despite the phenotypical and serological characteristics of the disease. The discovery of anti-aquaporin-4 antibody (AQP4-Ab) enabled clinicians to diagnose NMOSD relatively earlier and more easily, as the AQP4-Ab can mediate the pathogenesis of NMOSD. Testing for AQP4-Ab in the serum of patients can play a crucial role in the diagnosis of NMOSD. Three-quarters of patients with NMOSD have serum immunoglobulin-G (IgG) autoantibodies to the AQP4 channel. Nevertheless, the test results for AQP4-Ab can be affected by several factors, such as assay methods, clinical stages, the types of treatment, sample status, and pre-test error, among others. In patients with seronegative NMOSD, it would be better to test serum and CSF AQP4-Ab together to improve the positive rate, especially when NMOSD is highly suspected.