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In bacterial meningitis, chemokines lead to recruitment of polymorphonuclear leucocytes (PMN) into the CNS. At the site of infection in the subarachnoid space, PMN release reactive oxygen species, reactive nitrogen intermediates (RNI) and interleukin-1 beta (IL-1 beta). Although these immune factors assist in clearance of bacteria, they also result in neuronal injury associated with meningitis. Tr
