Conclusions
miR146a and miR132 may take part in the pathogenesis of SP bacterial meningitis as well as the TLR4- NFκB- TNF-α/IL1B signal transduction pathway.
Material and methods
Streptococcus pneumoniae induced rat meningitis models were taken and divided into 2 groups; control (C) and meningitis (M). Western blot was used to detect toll like receptor 4 (TLR4), tumor necrosis factor α (TNF-α), interleukin 1B (IL1B), nuclear factor κB (NFκB) and real time polymerase chain reaction were used to detect the expression of miR146a, miR132, respectively.
Methods
Streptococcus pneumoniae induced rat meningitis models were taken and divided into 2 groups; control (C) and meningitis (M). Western blot was used to detect toll like receptor 4 (TLR4), tumor necrosis factor α (TNF-α), interleukin 1B (IL1B), nuclear factor κB (NFκB) and real time polymerase chain reaction were used to detect the expression of miR146a, miR132, respectively.
Results
We found that the expressions of TLR4, TNF-α, IL1B, NFκB were all up-regulated in the acute stage of bacterial meningitis when compared to the control group. While for the post transcription factors, miR146a and miR132, the opposite was observed. They were down-regulated in the meningitis group. Conclusions: miR146a and miR132 may take part in the pathogenesis of SP bacterial meningitis as well as the TLR4- NFκB- TNF-α/IL1B signal transduction pathway.
