Cerebrospinal fluid concentrations of interleukin-1 beta, tumour necrosis factor-alpha, and interferon gamma in bacterial meningitis.

Ohga, Shouichi; Aoki, Takeshi; Okada, Kenji; Akeda, Hideki; Fujioka, Koji; Ohshima, Akira; Mori, T.; Minamishima, Ikuko; Ueda, Kohji

doi:10.1136/adc.70.2.123

Cited by 77 publications

(50 citation statements)

References 20 publications

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“…Previous reports diverge on the role of IFN-␥ in bacterial meningitis (43)(44)(45)(46); however, in our model IFN-␥ levels are not up-regulated during meningitis. Therefore, we cannot speculate on the interaction between IL-1 and IFN-␥.…”

Section: Discussioncontrasting

confidence: 45%

IL-1 Receptor Type 1 Gene-Deficient Mice Demonstrate an Impaired Host Defense Against Pneumococcal Meningitis

Zwijnenburg

Poll²,

Florquin

et al. 2003

The Journal of Immunology

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The fatality rate associated with Streptococcus pneumoniae meningitis remains high despite adequate antibiotic treatment. IL-1 is an important proinflammatory cytokine, which is up-regulated in brain tissue after the induction of meningitis. To determine the role of IL-1 in pneumococcal meningitis we induced meningitis by intranasal inoculation with 8 × 104 CFU of S. pneumoniae and 180 U of hyaluronidase in IL-1R type I gene-deficient (IL-1R−/−) mice and wild-type mice. Meningitis resulted in elevated IL-1α and IL-1β mRNA and protein levels in the brain. The absence of an intact IL-1 signal was associated with a higher susceptibility to develop meningitis. Furthermore, the lack of IL-1 impaired bacterial clearance, as reflected by an increased number of CFU in cerebrospinal fluid of IL-1R−/− mice. The characteristic pleocytosis of meningitis was not significantly altered in IL-1R−/− mice, but meningitis was associated with lower brain levels of cytokines. The mortality was significantly higher and earlier in the course of the disease in IL-1R−/− mice. These results demonstrate that endogenous IL-1 is required for an adequate host defense in pneumococcal meningitis.

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Section: Discussioncontrasting

confidence: 45%

IL-1 Receptor Type 1 Gene-Deficient Mice Demonstrate an Impaired Host Defense Against Pneumococcal Meningitis

Zwijnenburg

Poll²,

Florquin

et al. 2003

The Journal of Immunology

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“…Meningococcal meningitis is characterized by the presence of high levels of proinflammatory cytokines, including MC58 siaD + 1 mM SB202190 7.24 ± 2.9 1.18 ± 1.04 MC58 siaD + 10 mM SB202190 10.4 ± 4.9 1.33 ± 1.2 MC58 siaD + 20 mM SB202190 9.1 ± 5.7 1.28 ± 1.17 tumour necrosis factor-alpha (TNF-a), IL-1b, IL-6 and the CXC chemokine IL-8 (CXCL8) in the CSF (Waage et al, 1989;Ohga et al, 1994;van Deuren et al, 1995). A various number of bacterial surface components -in particular the lipooligosaccharide (LOS) -have been implicated in the release of cytokines induced by N. meningitidis in different cell types (Dixon et al, 2001;Kolb-Mäurer et al, 2001;Christodoulides et al, 2002;Unkmeir et al, 2002b).…”

Section: Activation Of P38 Mapk Is Implicated In N Meningitidisinducmentioning

confidence: 99%

Interaction of Neisseria meningitidis with human brain microvascular endothelial cells: role of MAP- and tyrosine kinases in invasion and inflammatory cytokine release

et al. 2004

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“…Early studies of S. pneumoniae meningitis showed the presence of IFN bioactivity in the cerebrospinal fluid (CSF) of patients with BM (35), but reports on the presence of IFN-g specifically are inconsistent, with some studies reporting concentrations that are low to undetectable (36)(37)(38)(39), whereas others suggested that IFN-g production may be present in at least some patients (40)(41)(42). Of particular note is the fact that many of these studies did not distinguish between causative agents when investigating the presence of IFN-g in CSF.…”

mentioning

confidence: 99%

Inflammasome-Dependent IFN-γ Drives Pathogenesis inStreptococcus pneumoniaeMeningitis

Mitchell

Yau

McQuillan

et al. 2012

The Journal of Immunology

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The pathology associated with Streptococcus pneumoniae meningitis results largely from activation of immune-associated pathways. We systematically investigated the production of IFN subtypes, as well as their influence on pathology, in a mouse model of S. pneumoniae meningitis. Despite the occurrence of a mixed IFN type I/II gene signature, no evidence for production or involvement of type I IFNs in disease progression was found. In contrast, type II IFN (IFN-γ) was strongly induced, and IFN-γ−/− mice were significantly protected from severe disease. Using intracellular cytokine staining and targeted cell-depletion approaches, NK cells were found to be the dominant source of IFN-γ. Furthermore, production of IFN-γ was found to be dependent upon ASC and IL-18, indicating that an ASC-dependent inflammasome pathway was responsible for mediating IFN-γ induction. The influence of IFN-γ gene deletion on a range of processes known to be involved in bacterial meningitis pathogenesis was examined. Although neutrophil numbers in the brain were similar in infected wild-type and IFN-γ−/− mice, both monocyte recruitment and CCL2 production were less in infected IFN-γ−/− mice compared with infected wild-type controls. Additionally, gene expression of NO synthase was strongly diminished in infected IFN-γ−/− mice compared with infected controls. Finally, bacterial clearance was enhanced in IFN-γ−/− mice, although the underlying mechanism remains unclear. Together, these data suggest that inflammasome-dependent IFN-γ contributes via multiple pathways to pathology during S. pneumoniae meningitis.

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Cerebrospinal fluid concentrations of interleukin-1 beta, tumour necrosis factor-alpha, and interferon gamma in bacterial meningitis.

Cited by 77 publications

References 20 publications

IL-1 Receptor Type 1 Gene-Deficient Mice Demonstrate an Impaired Host Defense Against Pneumococcal Meningitis

IL-1 Receptor Type 1 Gene-Deficient Mice Demonstrate an Impaired Host Defense Against Pneumococcal Meningitis

Interaction of Neisseria meningitidis with human brain microvascular endothelial cells: role of MAP- and tyrosine kinases in invasion and inflammatory cytokine release

Inflammasome-Dependent IFN-γ Drives Pathogenesis inStreptococcus pneumoniaeMeningitis

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