{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T05:46:21Z","timestamp":1792129581674,"version":"4.4.0"},"reference-count":59,"publisher":"Wiley","license":[{"start":{"date-parts":[[2013,1,1]],"date-time":"2013-01-01T00:00:00Z","timestamp":1356998400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"DOI":"10.13039\/501100013360","name":"Universidade do Extremo Sul Catarinense","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100013360","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Century NEL Masterclass American Smaller Companies"},{"DOI":"10.13039\/501100003593","name":"Conselho Nacional de Desenvolvimento Cient\u00edfico e Tecnol\u00f3gico","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003593","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100005667","name":"Funda\u00e7\u00e3o de Amparo \u00e0 Pesquisa e Inova\u00e7\u00e3o do Estado de Santa Catarina","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100005667","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Oxidative Medicine and Cellular Longevity"],"published-print":{"date-parts":[[2013]]},"abstract":"<jats:p>\n                    Pneumococcal meningitis is a life-threatening disease characterized by an acute purulent infection affecting the pia mater, the arachnoid, and the subarachnoid spaces.\n                    <jats:italic>Streptococcus pneumoniae<\/jats:italic>\n                    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-\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B-inducing kinase, resulting in the nuclear translocation of NF-\n                    <jats:italic>\u03ba<\/jats:italic>\n                    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\n                    <jats:sup>\u2022<\/jats:sup>\n                    ,\n                    <mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M1\">\n                      <mml:mrow>\n                        <mml:msup>\n                          <mml:mrow>\n                            <mml:msub>\n                              <mml:mrow>\n                                <mml:mtext>O<\/mml:mtext>\n                              <\/mml:mrow>\n                              <mml:mrow>\n                                <mml:mtext>2<\/mml:mtext>\n                              <\/mml:mrow>\n                            <\/mml:msub>\n                          <\/mml:mrow>\n                          <mml:mrow>\n                            <mml:mi>\u2022<\/mml:mi>\n                          <\/mml:mrow>\n                        <\/mml:msup>\n                      <\/mml:mrow>\n                    <\/mml:math>\n                    , and H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    . This formation generates oxidative and nitrosative stress, subsequently, lipid peroxidation, mitochondrial damage, and BBB breakdown, which contributes to cell injury during pneumococcal meningitis.\n                  <\/jats:p>","DOI":"10.1155\/2013\/371465","type":"journal-article","created":{"date-parts":[[2013,5,9]],"date-time":"2013-05-09T17:03:49Z","timestamp":1368119029000},"page":"1-7","source":"Crossref","is-referenced-by-count":47,"title":["Role of Oxidative Stress in the Pathophysiology of Pneumococcal Meningitis"],"prefix":"10.1155","volume":"2013","author":[{"given":"Tatiana","family":"Barichello","sequence":"first","affiliation":[{"name":"Laborat\u00f3rio de Microbiologia Experimental, Programa de P\u00f3s-Gradua\u00e7\u00e3o em Ci\u00eancias da Sa\u00fade, Unidade Acad\u00eamica de Ci\u00eancias da Sa\u00fade, Universidade do Extremo Sul Catarinense, 888806-000 Crici\u00fama, SC, Brazil"},{"name":"Instituto Nacional de Ci\u00eancia e Tecnologia Translacional em Medicina 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