PMID- 23766853
OWN - NLM
STAT- MEDLINE
DCOM- 20140813
LR  - 20211021
IS  - 1942-0994 (Electronic)
IS  - 1942-0900 (Print)
IS  - 1942-0994 (Linking)
VI  - 2013
DP  - 2013
TI  - Role of oxidative stress in the pathophysiology of pneumococcal meningitis.
PG  - 371465
LID - 10.1155/2013/371465 [doi]
LID - 371465
AB  - Pneumococcal meningitis is a life-threatening disease characterized by an acute 
      purulent infection affecting the pia mater, the arachnoid, and the subarachnoid 
      spaces. Streptococcus pneumoniae crosses the blood-brain barrier (BBB) by both 
      transcellular traversal and disruption of the intraepithelial tight junctions to 
      allow intercellular traversal. During multiplication, pneumococci release their 
      bacterial products, which are highly immunogenic and may lead to an increased 
      inflammatory response in the host. Thus, these compounds are recognized by 
      antigen-presenting cells through the binding of toll-like receptors. These 
      receptors induce the activation of myeloid differentiation factor 88 (MyD88), 
      which interacts with various protein kinases, including IL-1 receptor-associated 
      kinase-4 (IRAK4), which is phosphorylated and dissociated from MyD88. These 
      products also interact with tumor necrosis factor receptor-associated factor 6 
      dependent signaling pathway (TRAF6). This cascade provides a link to NF- kappa 
      B-inducing kinase, resulting in the nuclear translocation of NF- kappa B leading to 
      the production of cytokines, chemokines, and other proinflammatory molecules in 
      response to bacterial stimuli. Consequently, polymorphonuclear cells are 
      attracted from the bloodstream and then activated, releasing large amounts of 
      NO(*), O2(*), and H2O2. This formation generates oxidative and nitrosative 
      stress, subsequently, lipid peroxidation, mitochondrial damage, and BBB 
      breakdown, which contributes to cell injury during pneumococcal meningitis.
FAU - Barichello, Tatiana
AU  - Barichello T
AD  - Laboratorio de Microbiologia Experimental, Programa de Pos-Graduacao em Ciencias 
      da Saude, Unidade Academica de Ciencias da Saude, Universidade do Extremo Sul 
      Catarinense, Criciuma, SC, Brazil. tba@unesc.net
FAU - Generoso, Jaqueline S
AU  - Generoso JS
FAU - Simoes, Lutiana R
AU  - Simoes LR
FAU - Elias, Samuel G
AU  - Elias SG
FAU - Quevedo, Joao
AU  - Quevedo J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20130509
PL  - United States
TA  - Oxid Med Cell Longev
JT  - Oxidative medicine and cellular longevity
JID - 101479826
SB  - IM
MH  - Animals
MH  - Blood-Brain Barrier/immunology/pathology/physiopathology
MH  - Cell Movement
MH  - Humans
MH  - Immunity, Innate/immunology
MH  - Leukocytes/pathology
MH  - Meningitis, Pneumococcal/immunology/microbiology/*pathology/*physiopathology
MH  - *Oxidative Stress
PMC - PMC3665263
EDAT- 2013/06/15 06:00
MHDA- 2014/08/15 06:00
PMCR- 2013/05/09
CRDT- 2013/06/15 06:00
PHST- 2013/03/06 00:00 [received]
PHST- 2013/04/18 00:00 [accepted]
PHST- 2013/06/15 06:00 [entrez]
PHST- 2013/06/15 06:00 [pubmed]
PHST- 2014/08/15 06:00 [medline]
PHST- 2013/05/09 00:00 [pmc-release]
AID - 10.1155/2013/371465 [doi]
PST - ppublish
SO  - Oxid Med Cell Longev. 2013;2013:371465. doi: 10.1155/2013/371465. Epub 2013 May 
      9.