Pili on meningococci from primary cultures of nasopharyngeal carriers and cerebrospinal fluid of patients with acute disease.

DeVoe, I W; Gilchrist, J. E.

doi:10.1084/jem.141.2.297

Cited by 93 publications

(60 citation statements)

References 10 publications

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“…Knowledge of the modulins expressed by N. lactamica and N. meningitidis is important for understanding how both organisms are likely to interact with human meningeal cells. In the present study, the phenotype of the meningococcus was similar to that of strains isolated from the CSF of patients with meningitis (19,52) in expressing capsule, pili, LPS, and the major outer membrane proteins PorA, PorB, Opa, Opc, and Rmp. To our knowledge, no information is available on the antigens expressed by Neisseria lactamica isolated from the CSF of patients with meningitis.…”

Section: Discussionmentioning

confidence: 57%

Comparison of the Inflammatory Responses of Human Meningeal Cells following Challenge withNeisseria lactamicaand withNeisseria meningitidis

et al. 2006

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The rationale for the present study was to determine how different species of bacteria interact with cells of the human meninges in order to gain information that would have broad relevance to understanding aspects of the innate immune response in the brain. Neisseria lactamica is an occasional cause of meningitis in humans, and in this study we investigated the in vitro interactions between N. lactamica and cells derived from the leptomeninges in comparison with the closely related organism Neisseria meningitidis, a major cause of meningitis worldwide. N. lactamica adhered specifically to meningioma cells, but the levels of adherence were generally lower than those with N. meningitidis. Meningioma cells challenged with N. lactamica and N. meningitidis secreted significant amounts of the proinflammatory cytokine interleukin-6 (IL-6), the C-X-C chemokine IL-8, and the C-C chemokines monocyte chemoattractant protein 1 (MCP-1) and RANTES, but it secreted very low levels of the cytokine growth factor granulocyte-macrophage colony-stimulating factor (GM-CSF). Thus, meningeal cells are involved in the innate host response to Neisseria species that are capable of entering the cerebrospinal fluid. The levels of IL-8 and MCP-1 secretion induced by both bacteria were essentially similar. By contrast, N. lactamica induced significantly lower levels of IL-6 than N. meningitidis. Challenge with the highest concentration of N. lactamica (10 8 CFU) induced a small but significant down-regulation of RANTES secretion, which was not observed with lower concentrations of bacteria. N. meningitidis (10 6 to 10 8 CFU) also down-regulated RANTES secretion, but this effect was significantly greater than that observed with N. lactamica. Although both bacteria were unable to invade meningeal cells directly, host cells remained viable on prolonged challenge with N. lactamica, whereas N. meningitidis induced death; the mechanism was overwhelming necrosis with no significant apoptosis. It is likely that differential expression of modulins between N. lactamica and N. meningitidis contributes to these observed differences in pathogenic potential.Meningitis, inflammation of the meninges that surround the brain and the spinal cord (63), is the most common serious infection of the central nervous system. In humans, the meninges comprise the pachymenix (dura mater) and the leptomeninges, which consists of the arachnoid and pia mater together with the trabeculae that traverse the cerebrospinal fluid (CSF)-filled subarachnoid space (SAS) (4, 25). The bacterial etiology of meningitis is broad, and susceptibility to the causative organisms varies with age, with different groups of organisms affecting neonates, children, and adults (28). Neonatal bacterial meningitis is due mainly to transmission of bacteria from the maternal genital tract to the newborn infant, and the main organisms that cause disease are Streptococcus agalactiae (group B hemolytic streptococcus) and Escherichia coli K1 (28, 47). After the neonatal period, the most common bacterial ...

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Section: Discussionmentioning

confidence: 57%

Comparison of the Inflammatory Responses of Human Meningeal Cells following Challenge withNeisseria lactamicaand withNeisseria meningitidis

et al. 2006

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“…Meningeal cell lines were characterized by phase-contrast microscopy and immunocytochemical analysis with antibodies directed against specific cellular markers and by the similar quantitative patterns of adherence of meningococci in challenge experiments over time (17). The N. meningitidis that is normally recovered from infected CSF is both capsulated (Cap ϩ ) and piliated (Pil ϩ ) (6,44). The meningioma cell lines were challenged with a high dose (approximately 2.5 ϫ 10 8 CFU per monolayer) of Cap ϩ Pil ϩ N. meningitidis strain MC58, and reverse transcriptase PCR was used to screen for up-regulation of a panel of proinflammatory cytokines and chemokines.…”

Section: Resultsmentioning

confidence: 99%

Interaction ofNeisseria meningitidiswith Human Meningeal Cells Induces the Secretion of a Distinct Group of Chemotactic, Proinflammatory, and Growth-Factor Cytokines

et al. 2002

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The interactions of Neisseria meningitidis with cells of the leptomeninges are pivotal events in the progression of bacterial leptomeningitis. An in vitro model based on the culture of human meningioma cells was used to investigate the role of the leptomeninges in the inflammatory response. Following challenge with meningococci, meningioma cells secreted specifically the proinflammatory cytokine interleukin-6 (IL-6), the CXC chemokine IL-8, the CC chemokines monocyte chemoattractant protein 1 (MCP-1) and regulated-upon-activation, normal-T-cell expressed and secreted protein (RANTES), and the cytokine growth factor granulocyte-macrophage colony-stimulating factor (GM-CSF). A temporal pattern of cytokine production was observed, with early secretion of IL-6, IL-8, and MCP-1 followed by later increases in RANTES and GM-CSF levels. IL-6 was induced equally by the interactions of piliated and nonpiliated meningococci, whereas lipopolysaccharide (LPS) had a minimal effect, suggesting that other, possibly secreted, bacterial components were responsible. Induction of IL-8 and MCP-1 also did not require adherence of bacteria to meningeal cells, but LPS was implicated. In contrast, efficient stimulation of RANTES by intact meningococci required pilus-mediated adherence, which served to deliver increased local concentrations of LPS onto the surface of meningeal cells. Secretion of GM-CSF was induced by pilus-mediated interactions but did not involve LPS. In addition, capsule expression had a specific inhibitory effect on GM-CSF secretion, which was not observed with IL-6, IL-8, MCP-1, or RANTES. Thus, the data demonstrate that cells of the leptomeninges are not inert but are active participants in the innate host response during leptomeningitis and that there is a complex relationship between expression of meningococcal components and cytokine induction.Meningitis, which is an inflammation of the meninges that surround the brain within the skull and the spinal cord within the spinal canal (56), is the most common infection of the central nervous system. In humans, the meninges comprise the pachymenix or dura mater (hard mother) and the leptomeninges, which consist of the arachnoid mater and pia mater together with the trabeculae that traverse the cerebrospinal fluid (CSF)-filled subarachnoid space (SAS) (2, 9, 56). Classical bacterial meningitis is predominantly a leptomeningitis, with little or no involvement of the dura mater or the underlying brain. The bacterial etiology of leptomeningitis is broad, and a wide variety of bacteria that gain access to the SAS can initiate an inflammatory response. Susceptibility to the various causative agents is age dependent, and a distinct group of species affect neonates compared to the species that affect subjects over 1 month old (13). After the neonatal period, the most common bacterial agents that cause pyogenic leptomeningitis are Haemophilus influenzae, Streptococcus pneumoniae, and Neisseria meningitidis (meningococci). In affluent countries, vaccines developed against H. inf...

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“…The observations that meningococci in the CSF of patients with acute disease carry fimbriae (20,21) suggest that other bacteria causing meningitis might also recognize binding sites within the brain.…”

Section: Discussionmentioning

confidence: 99%

Binding sites in the rat brain for Escherichia coli S fimbriae associated with neonatal meningitis.

Parkkinen¹,

Korhonen²,

Père³

et al. 1988

J. Clin. Invest.

122

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Escherichia coli strains that cause sepsis and meningitis in neonatal infants carry S fimbriae that bind to sialyl galactoside units of cell surface glycoproteins. To investigate the possible role of S fimbriae in determining the tissue tropism of neonatal meningitis, we have studied the presence of binding sites for S fimbriae in different tissues of the neonatal rat which is susceptible to meningitis caused by S-fimbriated E. coli. Purified S fimbriae were incubated on cryostat sections of different rat organs and their binding was assessed by indirect immunofluorescence. In the brain of the neonatal rat, S fimbriae specifically bound to the luminal surfaces of the vascular endothelium and of the epithelium lining the choroid plexuses and brain ventricles. The binding was completely inhibited by the trisaccharide NeuAca2-3Gafl-14Glc, a receptor analogue of S fimbriae, and by a preceding neuraminidase treatment of the sections. A recombinant E. coll strain expressing S fimbriae adhered in large numbers to the same tissue sites in the neonatal brain sections as did the purified fimbriae, whereas the nonfimbriated host strain and a recombinant strain expressing P fimbriae did not adhere to brain tissues. The results suggest that adhesion of S-fimbriated bacteria to the binding sites observed in the neonatal brain has a pathogenetic role during bacterial invasion from circulation into the cerebrospinal fluid.

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Pili on meningococci from primary cultures of nasopharyngeal carriers and cerebrospinal fluid of patients with acute disease.

Cited by 93 publications

References 10 publications

Comparison of the Inflammatory Responses of Human Meningeal Cells following Challenge withNeisseria lactamicaand withNeisseria meningitidis

Comparison of the Inflammatory Responses of Human Meningeal Cells following Challenge withNeisseria lactamicaand withNeisseria meningitidis

Interaction ofNeisseria meningitidiswith Human Meningeal Cells Induces the Secretion of a Distinct Group of Chemotactic, Proinflammatory, and Growth-Factor Cytokines

Binding sites in the rat brain for Escherichia coli S fimbriae associated with neonatal meningitis.

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