Abstract: To elucidate the role of innate immunity in the pathogenesis of meningitis, the effects of cerebrospinal fluid (CSF) and of sera from patients with bacterial and abacterial meningitis were studied on monocytes because of their resemblance in function with brain microglial cells. Monocytes were isolated from the mononuclear fraction of blood of healthy donors. They were incubated in growth medium single and in the presence of purified lipopolysaccharide or lipoteichoic acid of intact cells of Streptococcus pneumoniae and of samples of CSF and sera of patients. Samples were drawn from 10 patients with bacterial and 26 with abacterial meningitis. Concentrations of tumor necrosis factor α, interleukin (IL) 1β, IL-6, IL-10, IL-12, and interferon γ were estimated in cell supernatants by enzyme-linked immunosorbent assay and of procalcitonin by an immunochemiluminometric assay. It was found that the addition of CSF from patients with bacterial meningitis induced higher concentrations of IL-1β, IL-6, IL-10, IL-12, and procalcitonin than controls and than the addition of CSF from patients with abacterial meningitis. Intact cells of S. pneumoniae failed to elicit similar responses to CSF of patients. The presence of CSF from patients with abacterial meningitis induced higher levels of interferon γ and IL-6 than controls. It is concluded that cells of the innate immunity play a considerable role in the pathogenesis of meningitis. CSF triggering elicits cytokine responses that are higher in bacterial than abacterial meningitis; IL-1β, IL-6, IL-10, and procalcitonin are important mediators in bacterial meningitis and IL-6 and interferon γ in abacterial meningitis.
*Department of Neurology, †Fourth Department of Internal Medicine and ‡First Department of Paediatrics, University of Athens, Medical School, Greece.
Address correspondence and reprint requests to E.J. Giamarellos-Bourboulis, MD, PhD, Fourth Department of Internal Medicine, ATTIKON University Hospital, 1 Rimini Street, 124 64 Athens, Greece. E-mail: firstname.lastname@example.org.