Evidence map›Paper›PMID 9596705›Full record

ArticleInfection and immunity1998

Analysis of host cells associated with the Spv-mediated increased intracellular growth rate of Salmonella typhimurium in mice.

P A Gulig, T J Doyle, J A Hughes, H Matsui

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Infection and immunity, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
15.0field-weighted citation impact, top 1% 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

26 citing papers in PubMed, 78 citations in OpenAlex.

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  13. Salmonella pathogenicity and host adaptation in chicken-associated serovars.Microbiology and molecular biology reviews : MMBR · 2013
    Review
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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

4 authors at 2 institutions in 2 countries.

P A GuligDepartment of Molecular Genetics and Microbiology, University of Florida College of Medicine, Gainesville, Florida 32610-0266, USA. gulig@college.med.ufl.edu
T J Doyle
J A Hughes
H Matsui
Florida College · USUniversity of Florida · US

Funding

SALMONELLA TYPHIMURIUM VIRULENCE PLASMIDR01AI028421 · NIAID · UNIVERSITY OF FLORIDA · PI GULIG, PAUL A · 1996 to 1996
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SALMONELLA TYPHIMURIUM VIRULENCE PLASMIDR29AI028421 · NIAID · UNIVERSITY OF FLORIDA · PI GULIG, PAUL A · 1990 to 1994
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NIAID NIH HHS AI28421
6 · The paper itself

Abstract

The 90-kb virulence plasmid of Salmonella typhimurium encodes five spv genes which increase the growth rate of the bacteria within host cells within the first week of systemic infection of mice (P. A. Gulig and T. J. Doyle, Infect. Immun. 61:504-511, 1993). The presently described study was aimed at identifying the host cells associated with Spv-mediated virulence by manipulating the mouse host and the salmonellae. To test the effects of T cells and B cells on the Spv phenotype, salmonellae were orally inoculated into nude and SCID BALB/c mice. Relative to normal BALB/c mice, nude and SCID BALB/c mice were unaffected for splenic infection with either the Spv+ or Spv- S. typhimurium strains at 5 days postinoculation. When mice were pretreated with cyclophosphamide to induce granulocytopenia, there was a variable increase in total salmonella infection, but the relative splenic CFU of Spv+ versus Spv- S. typhimurium was not changed after oral inoculation. In contrast, depletion of macrophages from mice by treatment with cyclophosphamide plus liposomes containing dichloromethylene diphosphate resulted in equivalent virulence of Spv+ and Spv- salmonellae. To examine if the spv genes affected the growth of salmonellae in nonphagocytic cells, an invA::aphT mutation was transduced into Spv+ and Spv- S. typhimurium strains. InvA- Spv+ salmonellae were not significantly affected for splenic infection after subcutaneous inoculation compared with the wild-type strain, and InvA- Spv- salmonellae were only slightly attenuated relative to InvA+ Spv- salmonellae. Invasion-defective salmonellae still exhibited the Spv phenotype. Therefore, infection of nonphagocytes is not involved with the Spv virulence function. Taken together, these data demonstrate that macrophages are essential for suppressing the infection by Spv- S. typhimurium, by serving as the primary host cell for Spv-mediated intracellular replication and possibly by inhibiting the replication of salmonellae within other macrophages.

Indexed as

Virulence FactorsAgranulocytosisAnimalsBacterial ProteinsCyclophosphamideLymphocytesMacrophagesMiceMice, Inbred BALB CMice, Mutant StrainsMice, NudeMice, SCIDNeutrophilsPhenotypeSalmonella Infections, AnimalSalmonella typhimuriumBacterial ProteinsCyclophosphamideVirulence Factors

Identifiers

PMID9596705
PMCPMC108227
OpenAlexW2160184764

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.