Neuroinflammation in Bacterial Meningitis

Agyeman, Philipp; Grandgirard, Denis; Leib, Stephen (2017). Neuroinflammation in Bacterial Meningitis. In: Lyck, R; Enzmann, G (eds.) The Blood Brain Barrier and Inflammation. Progress in Inflammation Research (pp. 213-252). Springer Nature 10.1007/978-3-319-45514-3_10

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Under physiologic conditions, the brain is a microbiologically sterile site
and is protected from infection by highly specialized barriers, including the hard
bony skull, the tough dura mater, and the restrictive blood–brain barrier (BBB).
Host defense mechanisms in the central nervous system (CNS) are limited and
tightly regulated. Peripheral immune cells and plasma proteins are largely excluded from the brain parenchyma. Once they have breached the protective barriers and entered the CNS, bacteria multiply within the cerebrospinal fluid space (CSF) highly efficiently exhibiting similar kinetics as in vitro and reaching concentrations of up to 109 CFU/mL. In response to the multiplying bacteria and their components, i.e., cell wall fragments, lipopolysaccharides, teichoic and lipoteichoic acids, peptidoglycans, bacterial DNA, and other cytosolic factors, resident cells in the perivascular space and the meninges release pro-inflammatory signaling molecules. Tumor necrosis factor-α, interleukin-1β, and IL-6 are released early on and trigger a cascade of other inflammatory
mediators, including a variety of cytokines, chemokines, platelet-activating
factor, antimicrobial peptides, prostaglandins, matrix metalloproteinases, nitric oxide, and reactive oxygen species initiating a self-perpetuating inflammatory cascade. The immediate consequences of the intense inflammatory reaction are a massive influx of leukocytes, the breakdown of the blood–brain barrier with the formation of brain edema, and alterations of the cerebral blood flow. This overshooting inflammatory reaction to the invading pathogens causes damage to the brain parenchyma as collateral damage and is the driving pathophysiologic mechanism of inflammatory inner ear damage, brain cortical ischemic injury, and hippocampal apoptosis, the most frequent histopathological correlates of the neurofunctional sequelae of bacterial meningitis.

Item Type:

Book Section (Book Chapter)

Division/Institute:

04 Faculty of Medicine > Service Sector > Institute for Infectious Diseases
04 Faculty of Medicine > Service Sector > Institute for Infectious Diseases > Research
04 Faculty of Medicine > Department of Gynaecology, Paediatrics and Endocrinology (DFKE) > Clinic of Paediatric Medicine

UniBE Contributor:

Agyeman, Philipp; Grandgirard, Denis and Leib, Stephen

Subjects:

500 Science > 570 Life sciences; biology
600 Technology > 610 Medicine & health

ISBN:

978-3-319-45512-9

Series:

Progress in Inflammation Research

Publisher:

Springer Nature

Language:

English

Submitter:

Stephen Leib

Date Deposited:

15 Jan 2018 09:03

Last Modified:

23 Oct 2019 15:14

Publisher DOI:

10.1007/978-3-319-45514-3_10

BORIS DOI:

10.7892/boris.107724

URI:

https://boris.unibe.ch/id/eprint/107724

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