Pathomechanisms of bacterial meningitis based on transcriptome analysis: role of kynurenine 3-hydroxylase and galectin-3/-9 in brain injury

Inflammation of the subarachnoid and ventricular space contributes to thedevelopment of brain damage i.e. cortical necrosis and hippocampal apoptosis inpneumococcal meningitis (PM). Galectin-3 and -9 are known pro-inflammatorymediators and regulators of apoptosis. Here, the gene and protein expression profilefor both galectins was assessed in the disease progression of PM. The mRNA ofLgals3 and Lgals9 increased continuously in the cortex and in the hippocampus from22 h to 44 h after infection. At 44 h after infection, mRNA levels of Lgals9 in thehippocampus were 7-fold and those of Lgals3 were 30-fold higher than in controls(P< 0.01). Galectin-9 protein did not change, but a significant increase in galectin-3 incortex and hippocampus was observed with the duration of PM. Galectin-3 waslocalized to polymorphonuclear neutrophils, microglia, monocytes and macrophages,suggesting an involvement of galectin-3 in the neuroinflammatory processes leadingto brain damage in PM.