This TNF-α-mediated apoptotic transcriptional program appears to be a mechanism to limit over-activation of innate immune responses, common to other bacteria inducing meningitis [22, 25] and consistent with high production of Th2 anti-inflammatory cytokines, IL-6 and IL-10, but low levels of Th1 cytokines such as IL-1β and IFN. This evidence concerns the gene IL1B and infectious meningitis.