Frequency and properties of naturally occurring adherent piliated strains of Haemophilus influenzae type b

Mason, Edward O.; Kaplan, Sheldon L.; Wiedermann, Bernhard L.; Norrod, E. Pinina; Stenback, Wayne A.

doi:10.1128/iai.49.1.98-103.1985

Cited by 67 publications

(33 citation statements)

References 22 publications

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“…Both meningococci and E. coli IH3080 also expressed pili (> 99%), but these were absent on S. pneumoniae. Although the original CSF isolate of H. influenzae strain Eagen expressed pili, analysis by TEM demonstrated the absence of pili in this strain, which is consistent with other reports demonstrating the loss of pili as a result of in vitro cultivation (Apicella et al, 1984;Pichichero, 1984;Mason et al, 1985).…”

Section: Bacterial Strains and Growth Conditionssupporting

confidence: 90%

Different meningitis-causing bacteria induce distinct inflammatory responses on interaction with cells of the human meninges

Fowler

Weller

Heckels

et al. 2004

Cellular Microbiology

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SummaryThe interactions of bacterial pathogens with cells of the human leptomeninges are critical events in the progression of meningitis. An in vitro model based on the culture of human meningioma cells was used to investigate the interactions of the meningeal pathogens Escherichia coli K1, Haemophilus influenzae , Neisseria meningitidis and Streptococcus pneumoniae . A rank order of association with meningioma cells was observed, with N. meningitidis showing the highest levels of adherence, followed by E. coli , S. pneumoniae and H. influenzae . Neisseria meningitidis and H. influenzae did not invade meningioma cells or induce cell death, but induced a concentration-dependent secretion of inflammatory mediators. Neisseria meningitidis induced higher levels of IL-6, MCP-1, RANTES and GM-CSF than H. influenzae , but there was no significant difference in the levels of IL-8 induced by both pathogens. Streptococcus pneumoniae was also unable to invade meningioma cells, but low concentrations of bacteria failed to stimulate cytokine secretion. However, higher concentrations of pneumococci led to cell death. By contrast, only E. coli K1 invaded meningioma cells directly and induced rapid cell death before an inflammatory response could be induced. These data demonstrate that the interactions of different bacterial pathogens with human meningeal cells are distinct, and suggest that different intervention strategies may be needed in order to prevent the morbidity and mortality associated with bacterial meningitis.

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Section: Bacterial Strains and Growth Conditionssupporting

confidence: 90%

Different meningitis-causing bacteria induce distinct inflammatory responses on interaction with cells of the human meninges

Fowler

Weller

Heckels

et al. 2004

Cellular Microbiology

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“…Early on, investigators noted that expression of hemagglutinating pili was subject to reversible phase variation [74,75,184]. During natural infection with H. in£uenzae type b, nasopharyngeal isolates are often piliated, while their isogenic counterparts from systemic sites are virtually always non-piliated [185]. At the same time, systemic isolates can be enriched in vitro for piliated variants, which themselves can revert to non-piliated forms.…”

Section: Hemagglutinating Pilimentioning

confidence: 99%

Molecular determinants of the pathogenesis of disease due to non-typable Haemophilus influenzae

Rao¹

1999

FEMS Microbiology Reviews

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Non-typable Haemophilus influenzae is a common commensal organism in the human upper respiratory tract and an important cause of localized respiratory tract disease. The pathogenesis of disease begins with bacterial colonization of the nasopharynx, a process that involves establishment on the mucosal surface and evasion of local immune mechanisms. Under the proper circumstances, the organism spreads contiguously to the middle ear, the sinuses, or the lungs, and then stimulates a brisk inflammatory response, producing symptomatic infection. In this review, we summarize our present understanding of the molecular determinants of this sequence of events. Continued investigation of the molecular mechanism of non-typable H. influenzae pathogenicity should facilitate development of novel approaches to the treatment and prevention of H. influenzae disease.

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“…Bacterial factors that contribute to colonization of mucosal surfaces in vivo, however, are not well characterized. Fimbriae have been shown to mediate adhesion to human oropharyngeal epithelial cells, but nasopharygeal isolates cultured from children are frequently non-piliated (Mason et aL, 1985: van Ham et aL, 1989). In addition, a pilin-deficient strain was still able to persist in the nasopharynx, although at reduced numbers compared with the fimbriated parent strain, in a simian model of H. influenzae carriage (Weber et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Identification and characterization of a cell envelope protein of Haemophilus influenzae contributing to phase variation in colony opacity and nasopharyngeal colonization

Weiser

Chong

Greenberg

et al. 1995

Molecular Microbiology

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Haemophilus influenzae undergoes spontaneous phase variation in colony morphology. Organisms from transparent colonies efficiently colonize the nasopharynx in an infant rat model of H. influenzae carriage, whereas organisms from more opaque colonies are deficient at colonization. A genetic approach relying on the transformability of H. influenzae was used to identify a locus contributing to opacity variation. By screening a library of chomosomal DNA from an opaque variant of strain Rd, it was possible to isolate a single clone capable of transforming a transparent Rd host to a more opaque phenotype. A region containing two genes, designated oapA and oapB, was identified. The deduced amino acid sequence of oapB has similarity to a consensus sequence for bacterial lipoproteins. Genetically defined mutations in oapA were transformed into the transparent Rd to confirm that this gene is required for expression of the transparent colony phenotype. Although oapA lacks a signal sequence, gene fusions to phoA show that OapA is secreted in H. influenzae and undergoes phase variation in expression. Mutagenesis of oapA in strain Rd, and type b strain Eagan, resulted in loss of the ability to colonize the nasopharynx of infant rats. The type b mutant, however, was as virulent as its parent strain when inoculated intraperitoneally. This suggests that the contribution of OapA to pathogenesis is limited to events associated with colonization of the mucosal surface.

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Frequency and properties of naturally occurring adherent piliated strains of Haemophilus influenzae type b

Cited by 67 publications

References 22 publications

Different meningitis-causing bacteria induce distinct inflammatory responses on interaction with cells of the human meninges

Different meningitis-causing bacteria induce distinct inflammatory responses on interaction with cells of the human meninges

Molecular determinants of the pathogenesis of disease due to non-typable Haemophilus influenzae

Identification and characterization of a cell envelope protein of Haemophilus influenzae contributing to phase variation in colony opacity and nasopharyngeal colonization

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