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Meningitis represents a dangerous medical condition which targets the protective brain and spinal cord membranes known as meninges.Ultimately, regardless of the type of causative agent, the common outcome of this inflammatory pathway is multifactorial neuronal damage.The surface of these microbes contains pathogenic molecules called PAMPs (Pathogen-Associated Molecular Patterns) which activate specific immune receptors called Toll-Like Receptors (TLRs) particularly TLR2 and TLR4 that exist on nervous system cells and immune system cells.When the BBB is disrupted, there is an increase in permeability of the BBB that allows for the outflow of fluid and protein from the intravascular to the extravascular spaces surrounding the brain parenchyma leading to cerebral edema.Following the release of these effector cells within the brain, they produce both mediators and proinflammatory cytokines that induce vascular dilatation and increase the permeability of the intracranial blood vessel, contributing to increased ICP.The cerebrospinal fluid attracts leukocytes primarily neutrophils during meningitis development.

Meningitis represents a dangerous medical condition which targets the protective
brain and spinal cord membranes known as meninges. The inflammation develops
because of different microbial agents.
The central nervous system becomes infected by different microorganisms which
trigger identical inflammatory responses after they enter the brain and spinal cord
area. The disease shows identical symptoms between different types, but the
causative agents follow distinct paths to reach the meninges and produce different
levels of inflammation in the subarachnoid space.
Bacterial meningitis produces fast and severe inflammation, but viral meningitis
causes milder symptoms and fungal meningitis develops slowly into a chronic
condition.
The surface of these microbes contains pathogenic molecules called PAMPs
(Pathogen-Associated Molecular Patterns) which activate specific immune receptors
called Toll-Like Receptors (TLRs) particularly TLR2 and TLR4 that exist on nervous
system cells and immune system cells. The ac&va&on process starts specific cellular
pathways which produce an immediate and powerful inflammatory response in the
meninges.
The cerebrospinal fluid attracts leukocytes primarily neutrophils during meningitis
development. Nitric oxide (NO) and matrix metalloproteinases (MMPs) can be
produced by cells that affect the brain's blood-brain barrier (BBB). When the BBB is
disrupted, there is an increase in permeability of the BBB that allows for the outflow
of fluid and protein from the intravascular to the extravascular spaces surrounding
the brain parenchyma leading to cerebral edema.
Endothelial cells, macrophages that reside adjacent to blood vessels, and mast cells
are pro-inflammatory effector cells that are involved in the inflammatory cascade.
Following the release of these effector cells within the brain, they produce both
mediators and proinflammatory cytokines that induce vascular dilatation and
increase the permeability of the intracranial blood vessel, contributing to increased
ICP. The result is diminished blood flow and reduced oxygen into the brain
parenchyma which can lead to neuronal injury and functional impairment of the CNS.
Ultimately, regardless of the type of causative agent, the common outcome of this
inflammatory pathway is multifactorial neuronal damage.