Evidence map›Paper›PMID 15731051›Full record

ArticleInfection and immunity2005

Antibody against V antigen prevents Yop-dependent growth of Yersinia pestis.

Alexander V Philipovskiy, Clarissa Cowan, Christine R Wulff-Strobel, Sandra H Burnett, Edward J Kerschen, Donald A Cohen, Alan M Kaplan, Susan C Straley

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
6.1field-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

44 citing papers in PubMed, 70 citations in OpenAlex.

  1. Trial
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  15. Article
  16. Article
  17. Toward a molecular pathogenic pathway for Yersinia pestis YopM.Frontiers in cellular and infection microbiology · 2012
    Article
  18. Review
  19. Article
  20. Amino acid and structural variability of Yersinia pestis LcrV protein.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2010
    Article
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

8 authors at 1 institution in 1 country.

Alexander V PhilipovskiyDepartment of Microbiology, Immunology, and Molecular Genetics, University of Kentucky, Lexington, KY 40536-0298, USA.
Clarissa Cowan
Christine R Wulff-Strobel
Sandra H Burnett
Edward J Kerschen
Donald A Cohen
Alan M Kaplan
Susan C Straley
University of Kentucky · US

Funding

PLASMID PCD1-ENCODED VIRULENCE DETERMINANTS IN PLAGUER37AI021017 · NIAID · UNIVERSITY OF KENTUCKY · PI STRALEY, SUSAN C · 1995 to 2004
$1.9M
PLASMID PCD-ENCODED VIRULENCE DETERMINANTS IN PLAGUER01AI021017 · NIAID · UNIVERSITY OF KENTUCKY · PI STRALEY, SUSAN C · 1986 to 1994
–
NIAID NIH HHS AI21017NIAID NIH HHS R37 AI021017
6 · The paper itself

Abstract

The V antigen (LcrV) of the plague bacterium Yersinia pestis is a potent protective antigen that is under development as a vaccine component for humans. LcrV is multifunctional. On the bacterial surface it mediates delivery of a set of toxins called Yops into host cells, and as a released protein it can cause production of the immunosuppressive cytokine interleukin-10 (IL-10) and can inhibit chemotaxis of polymorphonuclear neutrophils. It is not known how these mechanisms of LcrV operate, what their relative importance is, when they function during plague, and which are critical to protection by antibody. This study investigated several of these issues. C57BL/6 mice, mice unable to express IL-10, or mice with the macrophage lineage eliminated were treated with a protective anti-LcrV antibody or a nonprotective antibody against YopM and infected intravenously by Y. pestis KIM5 or a strain that lacked the genes encoding all six effector Yops. Viable bacterial numbers were determined at various times. The data indicated that Yops were necessary for Yersinia growth after the bacteria had seeded liver and spleen. Anti-LcrV antibody prevented this growth, even in IL-10-/- mice, demonstrating that one protective mechanism for anti-LcrV antibody is independent of IL-10. Anti-LcrV antibody had no effect on persistence in organs of Y. pestis lacking effector Yops, even though the yersiniae could strongly express LcrV, suggesting that Yops are necessary for building sufficient bacterial numbers to produce enough LcrV for its immunosuppressive effects. In vitro assays showed that anti-LcrV antibody could partially block delivery of Yops and downstream effects of Yops in infected macrophage-like J774A.1 cells. However, cells of the macrophage lineage were found to be dispensable for protection by anti-LcrV antibody in spleen, although they contributed to protection in liver. Taken together, the data support the hypothesis that one protective effect of the antibody is to block delivery of Yops to host cells and prevent early bacterial growth. The findings also identified the macrophage lineage as one host cell type that mediates protection.

Indexed as

AnimalsAntibodies, BacterialAntigens, BacterialBacterial Outer Membrane ProteinsCell LineHumansInterleukin-10MacrophagesMiceMice, Inbred C57BLPlaguePore Forming Cytotoxic ProteinsRabbitsVirulenceYersinia pestisAntibodies, BacterialAntigens, BacterialBacterial Outer Membrane ProteinsInterleukin-10LcrV protein, YersiniaPore Forming Cytotoxic ProteinsyopM protein, Yersinia

Identifiers

PMID15731051
PMCPMC1064938
OpenAlexW2132083856

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.