Interaction of<i>Neisseria meningitidis</i>with the Components of the Blood‐Brain Barrier Correlates with an Increased Expression of PilC

Pron, B.; Taha, Muhamed‐Kheir; Rambaud, Caroline; Fournet, Jean‐Christophe; Pattey, Natacha; Monnet, Jean-Paul; Musílek, Martin; Béretti, Jean-Luc; Nassif, Xavier

doi:10.1086/514124

Cited by 117 publications

(90 citation statements)

References 24 publications

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“…This is consistent with the observation that plexitis is frequently observed in early meningitis. On the other hand, a recent study suggests that N. meningitidis cross the BBB at both the choroid plexus and the BMEC (Pron et al, 1997). N. meningitidis was found to attach to the endothelium of the choroid plexus and the meninges in a patient with meningitis.…”

Section: Site Of Transversalmentioning

confidence: 93%

“…N. meningitidis was found to attach to the endothelium of the choroid plexus and the meninges in a patient with meningitis. Pilusmediated adhesion appears to be required for bacterial attachment to the BMEC (Pron et al, 1997). Other bacteria including E. coli (Huang et al, 1995), Listeria monocytogenes (Parida et al, 1998;Wilson and Drevets, 1998), Group B streptococcus (Nizet et al, 1997), and S. pneumoniae (Ring et al, 1998) have been demonstrated to adhere to and invade the BMEC in vitro.…”

Section: Site Of Transversalmentioning

confidence: 99%

“…Meningococcal LPS and several surface proteins including pilin, Opa, Opc, and PilC have been known to bind to a variety of host cellular receptors (Jerse and Rest, 1997). A speci®c role in CNS invasion has been suggested for PilC (Pron et al, 1997). In contrast, little is known about molecular basis of CNS invasion in L. monocytogenes, although a number of virulenceassociated proteins have been identi®ed in this pathogen (Cossart and Lecuit, 1998).…”

Section: Bacterial Moleculesmentioning

confidence: 99%

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Molecular and cellular mechanisms for microbial entry into the CNS

Zhang¹,

Tuomanen²

1999

J Neurovirol

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A number of pathogenic microbes including neuroinvasive viruses, bacteria and parasites are capable of entry into the central nervous system (CNS) and cause a variety of clinical manifestations. The cellular and molecular mechanisms for the CNS invasion have been extensively studied in the last two decades. Viruses invade neurons and thereby cause encephalitis or peripheral neuritis, while bacteria enter the cerebrospinal¯uid (CSF) and cause meningitis. In contrast, the mechanisms for parasitic neuroinvasion are much more complex and less clear. The capabilities that enable these elite subsets of pathogens to engineer uptake into the CNS will be the subject of this review.

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Section: Site Of Transversalmentioning

confidence: 93%

Section: Site Of Transversalmentioning

confidence: 99%

Section: Bacterial Moleculesmentioning

confidence: 99%

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Molecular and cellular mechanisms for microbial entry into the CNS

Zhang¹,

Tuomanen²

1999

J Neurovirol

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“…ROU (group W135, ET37), is a pilus-bearing encapsulated isolate obtained from the cerebrospinal fluid of a 2-month-old human infant (Pron et al, 1997). Mutant strains used, kindly provided by V. Pelicic (Inserm U570, Paris, France), have been described previously (Geoffroy et al, 2003;Stojiljkovic et al, 1997).…”

Section: Methodsmentioning

confidence: 99%

Invasion of endothelial cells by Neisseria meningitidis requires cortactin recruitment by a phosphoinositide-3-kinase/Rac1 signalling pathway triggered by the lipo-oligosaccharide

Lambotin

Hoffmann

Laran-Chich

et al. 2005

Journal of Cell Science

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Type-IV-pilus-mediated adhesion of Neisseria meningitidis (also known as meningococcus) to human endothelial cells induces the formation of membrane protrusions leading to bacterial uptake. We have previously shown that these protrusions result from a Rho- and Cdc42-dependent cortical actin polymerization, and from the activation of the ErbB2 tyrosine-kinase receptor and the Src kinase, leading to tyrosine phosphorylation of cortactin. We report here that N. meningitidis mutants expressing a deglycosylated lipo-oligosaccharide are poorly invasive. These mutants show structurally altered actin polymerization. Moreover, although they efficiently recruit and activate ErbB2 and Src, these mutants are defective in the recruitment and phosphorylation of cortactin. We demonstrate that phosphorylated cortactin controls the cortical actin polymerization, which leads to membrane protrusion formation. In addition, we show that cortactin recruitment is dependent on the activation of a phosphoinositide-3-kinase/Rac1-GTPase signalling pathway, which is required for actin polymerization and internalization of N. meningitidis, and is not activated by the mutant strains. Altogether, these results define a new role for the lipo-oligosaccharide in triggering a phosphoinositide-3-kinase/Rac1 signalling required to elicit an efficient uptake of N. meningitidis in non-phagocytic cells.

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“…Strains of N. meningitidis were tested that represent the genetic diversity of this species according to multilocus sequence typing (MLST) (18). Their MLST assignments were: ST1 (subgroup I, strain B40), ST2 (subgroup VI, Z6835), ST4 (subgroup IV-1, Z5463, Z2491 [27]), ST5 (subgroup III, Z3524), ST8 (A4 cluster, BZ 10), ST11 (ET-37 complex, serogroup C: FAM18; serogroup W135: ROU [24]), ST25 (NG G40), ST30 (NG 4/88), ST32 (ET-5 complex, 44/76), ST41 (lineage 3, BZ 198); ST48 (BZ147), ST49 (297-0), ST60 (subgroup IX, 890592), and ST74 (ET-5 complex, MC58 [33]). Additional strains were N. meningitidis 8013, N. gonorrhoeae FA1090 and two strains of Neisseria lactamica (Z6793 and Z6784).…”

Section: Methodsmentioning

confidence: 99%

Molecular and Biological Analysis of Eight Genetic Islands That Distinguish Neisseria meningitidis from the Closely Related Pathogen Neisseria gonorrhoeae

et al. 2000

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The pathogenic species Neisseria meningitidis and Neisseria gonorrhoeae cause dramatically different diseases despite strong relatedness at the genetic and biochemical levels. N. meningitidis can cross the blood-brain barrier to cause meningitis and has a propensity for toxic septicemia unlike N. gonorrhoeae. We previously used subtractive hybridization to identify DNA sequences which might encode functions specific to bacteremia and invasion of the meninges because they are specific to N. meningitidis and absent from N. gonorrhoeae. In this report we show that these sequences mark eight genetic islands that range in size from 1.8 to 40 kb and whose chromosomal location is constant. Five of these genetic islands were conserved within a representative set of strains and/or carried genes with homologies to known virulence factors in other species. These were deleted, and the mutants were tested for correlates of virulence in vitro and in vivo. This strategy identified one island, region 8, which is needed to induce bacteremia in an infant rat model of meningococcal infection. Region 8 encodes a putative siderophore receptor and a disulfide oxidoreductase. None of the deleted mutants was modified in its resistance to the bactericidal effect of serum. Neither were the mutant strains altered in their ability to interact with endothelial cells, suggesting that such interactions are not encoded by large genetic islands in N. meningitidis.Neisseria meningitidis colonizes the nasopharynx, from which it can seed the bloodstream before crossing the blood-brain barrier (BBB) to cause meningitis. In contrast, Neisseria gonorrhoeae colonizes and invades the epithelium of the genitourinary tract, where it can cause a localized inflammation; bacteremia, though frequent, is asymptomatic and dissemination is rare. Thus, both species are capable of crossing a cellular barrier at their port-of-entry but they differ in their abilities to subsequently disseminate in the blood. The ability to induce intense and prolonged bacteremia is one of the prerequisites for a bacterial pathogen to cross the BBB. In contrast, the details of specific interactions with the cellular components of the BBB remain unclear. Therefore, in order to understand the mechanisms that allow N. meningitidis to cross the BBB, it will be necessary to identify the genes that are involved in bloodstream dissemination and/or specific interaction with the cellular components of the BBB. Such genes might be present in both N. meningitidis and N. gonorrhoeae but differ subtly in sequence or regulation, or they might be present in only one of the two species.Results from in vitro models have shown that most of the mechanisms mediating cellular interactions are common to both N. meningitidis and N. gonorrhoeae. On the other hand, several determinants have been identified that are specific to N. meningitidis: the polysaccharide capsule (8), the enzyme rotamase (26), the RTX toxin-like Frp proteins (29, 30), and a glutathione peroxidase (20). Of these, the capsule locus is ...

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Interaction ofNeisseria meningitidiswith the Components of the Blood‐Brain Barrier Correlates with an Increased Expression of PilC

Cited by 117 publications

References 24 publications

Molecular and cellular mechanisms for microbial entry into the CNS

Molecular and cellular mechanisms for microbial entry into the CNS

Invasion of endothelial cells by Neisseria meningitidis requires cortactin recruitment by a phosphoinositide-3-kinase/Rac1 signalling pathway triggered by the lipo-oligosaccharide

Molecular and Biological Analysis of Eight Genetic Islands That Distinguish Neisseria meningitidis from the Closely Related Pathogen Neisseria gonorrhoeae

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