156 research outputs found

    Vermont, Clementien

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    Laboratory Predictors of Meningococcal Disease And Vaccination in Children: studies on the host immune response against Neisseria meningitidis

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    __Abstract__ Neisseria meningitidis is a gram-negative diplococcus which was first identified by Anton Weichselbaum in 1887. Strains of N. meningitidis can be classified into serogroups based upon the different composition of its capsular polysaccharide. Thirteen serogroups have been identified, of which serogroups A, B, C, W135 and Y are responsible for invasive disease. Additional subclassification is based on the variability of two outer membrane proteins: PorB and PorA. Antigenic variation in PorB is responsible for classification of meningococci into serotypes, whereas PorA is responsible for serosubtyping (www.neisseria.org/nm/typing). The outer membrane of N. meningitidis also contains lipopolysaccharide (LPS). The variability of the core structure of LPS is the basis of classification of N. meningitidis into at least 12 different immunotypes. N. meningitidis is an exclusively human pathogen and asymptomatic nasopharyngeal carriage among the population is approximately 7-17%. The carriage rate increases up to 45% when estimated by the culture of tonsillar tissue harvested on tonsillectomy

    Bench-to-bedside review: genetic influences on meningococcal disease

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    This review discusses the possible involvement of a variety of genetic polymorphisms on the course of meningococcal disease. It has been shown that several common genetic polymorphisms can either influence the susceptibility to meningococcal disease or can account for a higher mortality rate in patients. Gene polymorphisms concerning antibody receptors, lipopolysaccharide (LPS) binding receptors or proteins, innate complement proteins as well as cytokines and hemostatic proteins are described. The study of genetic polymorphisms might provide important insights in the pathogenesis of meningococcal disease and could make it possible to identify individuals who are at risk of either contracting or dying from meningococcal disease

    Polymorphisms in PARP, IL1B, IL4, IL10, C11NH, DEFB1 and DEFA4 in meningococcal disease in three populations.

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    Objective: the pathogenesis of meningococcal infections involves activation of the complement system, pro- and anti-inflammatory mediators, antimicrobial peptides and apoptosis. We hypothesized that variations in genes encoding these products are involved in the susceptibility to and severity of pediatric meningococcal infections.Study design: polymorphisms in PARP, C1INH, IL4, IL10 and IL1B, DEFA4 and DEFB1 were analyzed in two independent Caucasian case control cohorts from the UK and the Netherlands and in a family based TDT cohort from the UKResults: in the UK case control cohort the DEFB1 -44 G/G homozygous genotype was overrepresented in patients with meningococcal disease compared to the G/C and C/C genotypes when combined (OR 1.57, 95% CI 1.12-2.20). The TDT analysis did not confirm this, but did find an association and linkage of the IL4 -524 and the C1INH 480 polymorphisms with susceptibility to meningococcal infection. Hematological failure was present more often in UK patients with the DEFB1 -44 G/G genotype compared to the C allele carriers (OR 2.17, 95% CI 1.22-3.85).Conclusions: additional studies are necessary to elucidate the conflicting results obtained for the DEFB1, IL4 and C1INH polymorphisms and their role in susceptibility to and severity of meningococcal diseas
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