Community-acquired bacterial meningitis
D van de Beek, M Brouwer, R Hasbun… - Nature reviews Disease …, 2016 - nature.com
Meningitis is an inflammation of the meninges and subarachnoid space that can also involve
the brain cortex and parenchyma. It can be acquired spontaneously in the community …
the brain cortex and parenchyma. It can be acquired spontaneously in the community …
Astrocytes are active players in cerebral innate immunity
C Farina, F Aloisi, E Meinl - Trends in immunology, 2007 - cell.com
Innate immunity is a constitutive component of the central nervous system (CNS) and relies
strongly on resident myeloid cells, the microglia. However, evidence is emerging that the …
strongly on resident myeloid cells, the microglia. However, evidence is emerging that the …
Pathogenesis and pathophysiology of pneumococcal meningitis
BB Mook-Kanamori, M Geldhoff… - Clinical microbiology …, 2011 - Am Soc Microbiol
Pneumococcal meningitis continues to be associated with high rates of mortality and long-
term neurological sequelae. The most common route of infection starts by nasopharyngeal …
term neurological sequelae. The most common route of infection starts by nasopharyngeal …
Toll-like receptors in health and disease in the brain: mechanisms and therapeutic potential
The discovery of mammalian TLRs (Toll-like receptors), first identified in 1997 based on their
homology with Drosophila Toll, greatly altered our understanding of how the innate immune …
homology with Drosophila Toll, greatly altered our understanding of how the innate immune …
Innate immunity and neuroinflammation in the CNS: The role of microglia in Toll‐like receptor‐mediated neuronal injury
S Lehnardt - Glia, 2010 - Wiley Online Library
Microglia are key players of the immune response in the central nervous system (CNS) and,
being the resident innate immune cells, they are responsible for the early control of …
being the resident innate immune cells, they are responsible for the early control of …
Insights into the interaction between influenza virus and pneumococcus
JA McCullers - Clinical microbiology reviews, 2006 - Am Soc Microbiol
Bacterial infections following influenza are an important cause of morbidity and mortality
worldwide. Based on the historical importance of pneumonia as a cause of death during …
worldwide. Based on the historical importance of pneumonia as a cause of death during …
Toll-like receptor 2 suppresses immunity against Candida albicans through induction of IL-10 and regulatory T cells
MG Netea, R Sutmuller, C Hermann… - The Journal of …, 2004 - journals.aai.org
Abstract Toll-like receptor (TLR) 2 and TLR4 play a pivotal role in recognition of Candida
albicans. We demonstrate that TLR2−/− mice are more resistant to disseminated Candida …
albicans. We demonstrate that TLR2−/− mice are more resistant to disseminated Candida …
Toll‐like receptors in central nervous system glial inflammation and homeostasis
T Kielian - Journal of neuroscience research, 2006 - Wiley Online Library
Toll‐like receptors (TLRs) are a family of pattern‐recognition receptors expressed on cells of
the innate immune system that allow for the recognition of conserved structural motifs on a …
the innate immune system that allow for the recognition of conserved structural motifs on a …
Recognition of microbial infection by Toll-like receptors
E Kopp, R Medzhitov - Current opinion in immunology, 2003 - Elsevier
The Toll-like receptors (TLRs) of the innate immune system detect host invasion by
pathogens and initiate immune responses. All of the TLRs use the adaptor MyD88 to …
pathogens and initiate immune responses. All of the TLRs use the adaptor MyD88 to …
Early release of HMGB-1 from neurons after the onset of brain ischemia
J Qiu, M Nishimura, Y Wang, JR Sims… - Journal of Cerebral …, 2008 - journals.sagepub.com
The nuclear protein high-mobility group box 1 (HMGB-1) promotes inflammation in sepsis,
but little is known about its role in brain ischemia-induced inflammation. We report that …
but little is known about its role in brain ischemia-induced inflammation. We report that …