Evidence map›Paper›PMID 20160017›Full record

ArticleInfection and immunity2010

Three surface exoglycosidases from Streptococcus pneumoniae, NanA, BgaA, and StrH, promote resistance to opsonophagocytic killing by human neutrophils.

Ankur B Dalia, Alistair J Standish, Jeffrey N Weiser

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
5.9field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

82 citing papers in PubMed, 128 citations in OpenAlex.

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  11. Combining the In Silico and In Vitro Assays to IdentifyPharmaceuticals (Basel, Switzerland) · 2023
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  12. Role ofFrontiers in cellular and infection microbiology · 2023
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  14. Diverse Mechanisms of Protective Anti-Pneumococcal Antibodies.Frontiers in cellular and infection microbiology · 2022
    Review
  15. Frontiers in cellular and infection microbiology · 2022
    Review
  16. Article
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22 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Ankur B DaliaDepartment of Microbiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Alistair J Standish
Jeffrey N Weiser
Pediatrics and Genetics · USUniversity of Pennsylvania · US

Funding

ROLE OF OPACITY VARIATION IN PNEUMOCOCCAL PATHOGENESISR01AI038446 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEISER, JEFFREY NEAL · 1996 to 2019
$7.4M
BACTERIAL PHOSPHORYLCHOLINE AND PATHOGENESISR01AI044231 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEISER, JEFFREY NEAL · 1999 to 2009
$2.6M
Bacterial phosphorycholine and pathogenesisR21AI044231 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI WEISER, JEFFREY N. · 2004 to 2004
$350k
NIAID NIH HHS AI38446NIAID NIH HHS AI44231NIAID NIH HHS R01 AI038446NIAID NIH HHS R01 AI044231NIAID NIH HHS R21 AI044231
6 · The paper itself

Abstract

Streptococcus pneumoniae (the pneumococcus) is a major human pathogen and a leading cause of inflammatory infections such as pneumonia and otitis media. An important mechanism for host defense against S. pneumoniae is opsonophagocytic killing by neutrophils. To persist in the human host, the pneumococcus has developed strategies to evade opsonization and subsequent neutrophil-mediated killing. Utilizing a genomic approach, we identified NanA, the major pneumococcal neuraminidase, as a factor important for resistance to opsonophagocytic killing in ex vivo killing assays using human neutrophils. The effect of NanA was shown using both type 4 (TIGR4) and type 6A clinical isolates. NanA promotes this resistance by acting in conjunction with two other surface-associated exoglycosidases, BgaA, a beta-galactosidase, and StrH, an N-acetylglucosaminidase. Experiments using human serum showed that these exoglycosidases reduced deposition of complement component C3 on the pneumococcal surface, providing a mechanism for this resistance. Additionally, we have shown that antibodies in human serum do not contribute to this phenotype. These results demonstrate that deglycosylation of a human serum glycoconjugate(s) by the combined effects of NanA, BgaA, and StrH, is important for resistance to complement deposition and subsequent phagocytic killing of S. pneumoniae.

Indexed as

Antibodies, BacterialBacterial ProteinsComplement C3Glycoside HydrolasesHumansMicrobial ViabilityNeutrophilsOpsonin ProteinsProtein BindingStreptococcus pneumoniaeVirulence FactorsAntibodies, BacterialBacterial ProteinsComplement C3Glycoside HydrolasesOpsonin ProteinsVirulence Factors

Identifiers

PMID20160017
PMCPMC2863504
OpenAlexW2150208534

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.