الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Meningitis is a serious disease, and it’s prognosis depends mainly on early diagnosis and the provisioning of immediate and adequate treatment.
Aseptic meningitis is a syndrome characterized by acute onset of signs and symptoms of meningeal inflammation, cerebrospinal fluid (CSF) pleocytosis and absence of microorganisms either on Gram stain or on routine culture. It has ,to some extent ,more benign clinical course, however, sometimes may be complicated with meningoencephalitis exhibiting more severe courses and outcomes.
CNS viral invasion may occur via several mechanisms. Once viral infection of the CNS occurs, the initial inflammatory response is immunologically specific. Sensitized lymphocytes probably respond to a virus specific protein that diffuses or is transported to the luminal surface of the endothelium, with subsequent passage through endothelial cells and release of inflammatory cytokines.
In response to cytokines cerebrovascular endothelial cells (CVEs) produce intercelluar adhesion molecules, vascular cell adhesion molecules, and matrix metalloproteinases, which enhances increasing permeability of the BBB, encouraging peripheral immune system cells the entry into the brain.
T cell responses appear to have a more superior role than B cell responses.CXCL13 is manufactured mainly by stromal cells and follicular denderitic cells (FDC) in B cell follicles, and recruits both B cells and CD4+ T follicular helper (Tfh) cells to these compartments via its cognate receptor, CXCR5. CSF CXCL13 levels are elevated in an acute phase of both aseptic and septic CNS infections.