Nitric oxide participates in the immune response against<i>Neisseria meningitidis</i>serogroup B

Padrón, Julio Rodríguez; Bebelagua, Yanín; Lastre, Miriam; Lapinet, José; Zayas, Caridad; Quintero, Yanet; Díaz, Miriam; Pérez, Oliver

doi:10.1111/j.1574-695x.1999.tb01364.x

Cited by 3 publications

(3 citation statements)

References 22 publications

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“…2A). However, at later time points (24,48, and 72 h p.i. ), the level of bac-teremia for TLR9 Ϫ/Ϫ mice was significantly higher than that for C57BL/6 mice ( Fig.…”

Section: Resultsmentioning

confidence: 99%

“…One way through which macrophages kill meningococci is through production of reactive nitrogen and oxygen radicals (24,33). To test if the production of NO in response to meningococcal infection was dependent on either TLR2 or TLR9, we harvested and cultured peritoneal macrophages and spleen cells from C57BL/6, TLR2 Ϫ/Ϫ , TLR9 Ϫ/Ϫ , and TLR2/9 Ϫ/Ϫ mice and treated them as indicated in Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Infection with N. meningitidis triggers an innate immune response aimed at eliminating the pathogen. Host factors known to contribute to restriction of N. meningitidis include the complement system (23), antimicrobial peptides (7), reactive nitrogen and oxygen radicals (24,33), and a number of components of the inflammatory response (9). However, the potent inflammatory response evoked by invasive N. meningitidis infection is also associated with development of disease and is responsible for some of the severe symptoms characteristic of meningococcal disease (29).…”

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Important Role for Toll-Like Receptor 9 in Host Defense against Meningococcal Sepsis

et al. 2008

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Neisseria meningitidis is a leading cause of meningitis and sepsis. The pathogenesis of meningococcal disease is determined by both bacterial virulence factors and the host inflammatory response. Toll-like receptors (TLRs) are prominent activators of the inflammatory response, and TLR2, -4, and -9 have been reported to be involved in the host response to N. meningitidis. While TLR4 has been suggested to play an important role in early containment of infection, the roles of TLR2 and TLR9 in meningococcal disease are not well described. Using a model for meningococcal sepsis, we report that TLR9 ؊/؊ mice displayed reduced survival and elevated levels of bacteremia compared to wild-type mice. In contrast, TLR2؊/؊ mice controlled the infection in a manner comparable to that of wild-type mice. TLR9 deficiency was also associated with reduced bactericidal activity in vitro, which was accompanied by reduced production of nitric oxide by TLR9-deficient macrophages. Interestingly, TLR9؊/؊ mice recruited more macrophages to the bloodstream than wild-type mice and produced elevated levels of cytokines at late time points during infection. At the cellular level, activation of signal transduction and induction of cytokine gene expression were independent of TLR2 or TLR9 in macrophages and conventional dendritic cells. In contrast, plasmacytoid dendritic cells relied entirely on TLR9 to induce these activities. Thus, our data demonstrate an important role for TLR9 in host defense against N. meningitidis.

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“…2A). However, at later time points (24,48, and 72 h p.i. ), the level of bac-teremia for TLR9 Ϫ/Ϫ mice was significantly higher than that for C57BL/6 mice ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

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Important Role for Toll-Like Receptor 9 in Host Defense against Meningococcal Sepsis

et al. 2008

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Fur functions as an activator and as a repressor of putative virulence genes in Neisseria meningitidis

Delany

Rappuoli

Scarlato

2004

Molecular Microbiology

165

155

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SummaryFur is a well-known iron-responsive repressor of gene transcription, which is used by many bacteria to respond to the low-iron environment that pathogens encounter during infection. Four promoters of Neisseria meningitidis predicted to have Fur-binding boxes were selected to study the molecular interactions between Fur and the promoter regions of genes expected to play a central role in survival and pathogenesis. We demonstrate that Fur acts not only as a repressor, but also as an activator of gene expression both in vivo and in vitro . We report that Fur binds to operators located upstream of three promoters that are positively regulated in vivo by Fur and iron, whereas Fur binds to an operator overlapping the classically iron-repressed tbp promoter. Deletion of the upstream operator in the norB promoter abolished activation of transcription in vivo in response to iron and in vitro in response to Fur. The role of such a dual mechanism of Fur regulation during infection is discussed.

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Genome-wide transcriptional profiling of Neisseria Meningitidis in ex vivo models of Septicaemia

Hedman¹

2009

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Nitric oxide participates in the immune response againstNeisseria meningitidisserogroup B

Cited by 3 publications

References 22 publications

Important Role for Toll-Like Receptor 9 in Host Defense against Meningococcal Sepsis

Important Role for Toll-Like Receptor 9 in Host Defense against Meningococcal Sepsis

Fur functions as an activator and as a repressor of putative virulence genes in Neisseria meningitidis

Genome-wide transcriptional profiling of Neisseria Meningitidis in ex vivo models of Septicaemia

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