Abstract
Infections of the central nervous system (CNS) are still a major cause of morbidity and mortality worldwide. Traversal of the barriers protecting the brain by pathogens is a prerequisite for the development of meningitis. Bacteria have developed a variety of different strategies to cross these barriers and reach the CNS. To this end, they use a variety of different virulence factors that enable them to attach to and traverse these barriers. These virulence factors mediate adhesion to and invasion into host cells, intracellular survival, induction of host cell signaling and inflammatory response, and affect barrier function. While some of these mechanisms differ, others are shared by multiple pathogens. Further understanding of these processes, with special emphasis on the difference between the blood–brain barrier and the blood–cerebrospinal fluid barrier, as well as virulence factors used by the pathogens, is still needed.
Highlights
Bacterial meningitis, as are bacterial encephalitis and meningoencephalitis, is an inflammatory disease of the central nervous system (CNS)
The traversal or breach of these barriers by meningitis-causing pathogens is defined by a complex interplay between host cells and the pathogens, which use an array of virulence factors to facilitate this interaction, resulting in high morbidity and mortality [1]
Another major barrier protecting the brain is the blood–cerebrospinal fluid barrier (BCSFB), which can be separated into a barrier to the inner CSF in the ventricles at the choroid plexus (CP) and barriers to the outer CSF located at the arachnoidea and blood vessels present in the subarachnoidal space [15]
Summary
As are bacterial encephalitis and meningoencephalitis, is an inflammatory disease of the central nervous system (CNS). The traversal or breach of these barriers by meningitis-causing pathogens is defined by a complex interplay between host cells and the pathogens, which use an array of virulence factors to facilitate this interaction, resulting in high morbidity and mortality [1]. These virulence factors are involved during protection in the bloodstream, such as the capsule of both gram-positive and gram-negative bacteria, mediate adhesion to and invasion into host cells, and are responsible for intracellular survival
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