Abstract
Meningitis, the inflammation of the protective membrane surrounding the brain and spinal cord (known as meninges), is a condition associated with high mortality rates and permanent neurological sequelae in a significant proportion of survivors. The opportunistic pathogen Streptococcus pneumoniae (SPN/pneumococcus) is the leading cause of bacterial meningitis in adults and older children. Following infection of the lower respiratory tract and subsequent bloodstream invasion, SPN breaches the blood–brain barrier endothelium for invasion of the central nervous system. Transcytosis, a mode of passage through the endothelial cells has been identified as the predominant route of pneumococcal blood–brain barrier trafficking. Herein, we review the interactions enabling SPN invasion into the brain endothelial cells, events involved in the tug-of-war between pneumococcal virulence factors and host intracellular defense machineries and pneumococcal strategies for evasion of host defenses and successful transendothelial trafficking.
Highlights
Anjali Anil and Anirban Banerjee*Specialty section: This article was submitted to Bacteria and Host, a section of the journal Frontiers in Cellular and Infection
The central nervous system (CNS) consists primarily of the brain, the control center of the body, and the spinal cord, enveloped in meninges and protected by the skull and vertebrae, respectively
The tight junctions composed of claudins, occludins and junction adhesion molecules are present toward the apical side of the barrier and, along with the adherens junctions, contributes to the high transendothelial electrical resistance and dictates polarity to the blood–brain barrier (BBB) endothelium (Sandoval and Witt, 2008; Luissint et al, 2012)
Summary
Specialty section: This article was submitted to Bacteria and Host, a section of the journal Frontiers in Cellular and Infection. The opportunistic pathogen Streptococcus pneumoniae (SPN/pneumococcus) is the leading cause of bacterial meningitis in adults and older children. Following infection of the lower respiratory tract and subsequent bloodstream invasion, SPN breaches the blood–brain barrier endothelium for invasion of the central nervous system. Transcytosis, a mode of passage through the endothelial cells has been identified as the predominant route of pneumococcal blood–brain barrier trafficking. We review the interactions enabling SPN invasion into the brain endothelial cells, events involved in the tug-of-war between pneumococcal virulence factors and host intracellular defense machineries and pneumococcal strategies for evasion of host defenses and successful transendothelial trafficking
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