Abstract
Bacterial meningitis is a complex disorder in which injury is caused, in part, by the causative organism and, in part, by the host's own inflammatory response. Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine and a neuro-endocrine mediator that might play a role in pneumococcal meningitis. Here, we discuss the role of MIF in infection, the brain, and corticosteroids and conclude that experimental meningitis studies have to determine whether MIF is a potential target for adjunctive therapy in pneumococcal meningitis.
Highlights
migration inhibitory factor (MIF) is a multi-functional protein that acts both as a cytokine [2] and a neuro-endocrine mediator [3]
As a neuro-endocrine mediator, MIF is secreted by anterior pituitary cells in response to low serum glucocorticoids levels, thereby overriding the inhibitory effect of glucocorticoids on the immune response [3]
Care, the mortality due to pneumococcal meningitis ranges from 16% to 37% and neurological sequelae are estimated to occur in 30% to 52% of surviving adults [10]
Summary
MIF is a multi-functional protein that acts both as a cytokine [2] and a neuro-endocrine mediator [3]. MIF has been reported to play a role in the pathogenesis of several inflammatory and infectious diseases, including sepsis and septic shock [5]. As a neuro-endocrine mediator, MIF is secreted by anterior pituitary cells in response to low serum glucocorticoids levels, thereby overriding the inhibitory effect of glucocorticoids on the immune response [3]. At high glucocorticoid levels, MIF is no longer able to effectively limit corticosteroid-mediated pathways, thereby preventing an excessive and potentially harmful immune response [5].
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