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Oxidative Medicine and Cellular LongevityVolume 2013 2013, Article ID 371465, 7 pages

Review Article

Laboratório de Microbiologia Experimental, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, 888806-000 Criciúma, SC, Brazil

Instituto Nacional de Ciência e Tecnologia Translacional em Medicina INCT-TM, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, 88806-000 Criciúma, SC, Brazil

Núcleo de Excelência em Neurociências Aplicadas de Santa Catarina NENASC, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, 88806-000 Criciúma, SC, Brazil

Laboratório de Neurociências, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, 888806-000 Criciúma, SC, Brazil

Received 6 March 2013; Accepted 18 April 2013

Academic Editor: Francisco Javier Romero

Copyright © 2013 Tatiana Barichello et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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-κB-inducing kinase, resulting in the nuclear translocation of NF-κB 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

, , 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.





Autor: Tatiana Barichello, Jaqueline S. Generoso, Lutiana R. Simões, Samuel G. Elias, and João Quevedo

Fuente: https://www.hindawi.com/



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