Neuraminidase activities of clinical isolates of Diplococcus pneumoniae

Kelly, Richard T.; Farmer, Sawyer; Greiff, Donald

doi:10.1128/jb.94.1.272-273.1967

Cited by 55 publications

(23 citation statements)

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“…Although recovery was not demonstrated, the cause of embryonic death was very likely due mainly to the accumulation of toxic substances derived from the pneumococci. Elucidation of these toxic substances has been undertaken by several investigators, and further studies are required to solve this problem (5,7,8). In this regard, the much greater survival rate following Haemophilus infection would seem to emphasize the marked toxicity of pneumococci for the chick embryo.…”

Section: Discussionmentioning

confidence: 99%

Experimental Pneumococcal Infection in Embryonated Eggs Previously Infected with Influenza C Virus

Blouse

Buddingh

1972

Infect Immun

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Cumulative mortality rates for embryonated eggs, compiled for a variety of pneumococcal strains, indicated a uniformly high degree of virulence. Based on median lethal dose values for combined infection with influenza C virus and single infection with pneumococcus, it is difficult to conclude that pneumococcal virulence is enhanced in combined infection. However, there was a significant increase in mortality during the first 24 hr following combined infection. A significantly greater in vitro growth rate for pneumococcus was shown in amniotic fluid from virusinfected embryonated eggs. Microscopy study of selected embryos revealed the absence of a discernible inflammatory reaction during the first 24 hr. From 48 through 96 hr after inoculation, inflammatory reactions were restricted to the upper and lower respiratory tract and consisted of a polymorphonuclear leukocyte infiltration in response to the localization of pneumococci in the paranasal sinuses, bronchi, alveolar ducts, and alveolar spaces. Extensive, severe inflammatory reactions were more frequently encountered in the combined infection. The various phases from early exudation to eventual resolution, which characterize pneumococcal pneumonia in the human host, were in clear evidence following both the single and combined infection of the chick embryo.

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Section: Discussionmentioning

confidence: 99%

Experimental Pneumococcal Infection in Embryonated Eggs Previously Infected with Influenza C Virus

Blouse

Buddingh

1972

Infect Immun

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“…It is responsible for frequently occurring diseases including pneumonia, otitis media, sinusitis and meningitis. All SPN strains tested have been shown to possess neuraminidase (sialidase) activity (Kelly et al, 1967). Although three distinct neuraminidases, nanA, nanB and nanC, are present in the SPN genome (Xu et al, 2008), only NanA is surfaced-anchored and present in all strains (Camara et al, 1994;King et al, 2005;Pettigrew et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Activation of brain endothelium by pneumococcal neuraminidase NanA promotes bacterial internalization

Banerjee

Sorge

Sheen

et al. 2010

Cellular Microbiology

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SummaryStreptococcus pneumoniae (SPN), the leading cause of meningitis in children and adults worldwide, is associated with an overwhelming host inflammatory response and subsequent brain injury. Here we examine the global response of the blood-brain barrier to SPN infection and the role of neuraminidase A (NanA), an SPN surface anchored protein recently described to promote central nervous system tropism. Microarray analysis of human brain microvascular endothelial cells (hBMEC) during infection with SPN or an isogenic NanA-deficient (DnanA) mutant revealed differentially activated genes, including neutrophil chemoattractants IL-8, CXCL-1, CXCL-2. Studies using bacterial mutants, purified recombinant NanA proteins and in vivo neutrophil chemotaxis assays indicated that pneumococcal NanA is necessary and sufficient to activate host chemokine expression and neutrophil recruitment during infection. Chemokine induction was mapped to the NanA N-terminal lectin-binding domain with a limited contribution of the sialidase catalytic activity, and was not dependent on the invasive capability of the organism. Furthermore, pretreatment of hBMEC with recombinant NanA protein significantly increased bacterial invasion, suggesting that NanA-mediated activation of hBMEC is a prerequisite for efficient SPN invasion. These findings were corroborated in an acute murine infection model where we observed less inflammatory infiltrate and decreased chemokine expression following infection with the DnanA mutant.

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“…It produces several factors which are of possible relevance in the pathogenesis of disease. One of these is neuraminidase, an enzyme which cleaves N-acetylneuraminic acid (NeuNAc) from mucin, glycoproteins, and gangliosides (8,17). Although the role of neuraminidase is unclear, there is some indirect evidence to suggest that it may function as a pneumococcal virulence factor.…”

mentioning

confidence: 99%

“…Although the role of neuraminidase is unclear, there is some indirect evidence to suggest that it may function as a pneumococcal virulence factor. For example, all clinical isolates produce neuraminidase (8,14), and intracerebral inoculation of mice with partially purified neuraminidase caused neurological disease signs and death (7). However, these symptoms were not apparent on intrathecal inoculation of the enzyme in dogs (15).…”

mentioning

confidence: 99%

Streptococcus pneumoniae produces at least two distinct enzymes with neuraminidase activity: cloning and expression of a second neuraminidase gene in Escherichia coli

et al. 1991

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A gene from Streptococcus pneumoniae was cloned in lambda EMBL301 and then expressed in Escherichia coli, which cleaved the fluorogenic neuraminidase substrate 2'-(4-methylumbelliferyl)-alpha-d-N-acetylneuraminic acid. The cloned gene therefore encodes an enzyme with neuraminidase activity. On the basis of restriction mapping and DNA hybridization studies, this gene could be distinguished from another pneumococcal neuraminidase gene cloned previously (A. M. Berry, J. C. Paton, E. M. Glare, D. Hansman, and D. E. A. Catcheside, Gene 71:299-305, 1988). Both neuraminidase genes were found in each of five isolates, covering at least three serotypes, of pneumococci tested.

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Neuraminidase activities of clinical isolates of Diplococcus pneumoniae

Cited by 55 publications

References 0 publications

Experimental Pneumococcal Infection in Embryonated Eggs Previously Infected with Influenza C Virus

Experimental Pneumococcal Infection in Embryonated Eggs Previously Infected with Influenza C Virus

Activation of brain endothelium by pneumococcal neuraminidase NanA promotes bacterial internalization

Streptococcus pneumoniae produces at least two distinct enzymes with neuraminidase activity: cloning and expression of a second neuraminidase gene in Escherichia coli

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