Evidence map›Paper›PMID 8418038›Full record

ArticleInfection and immunity1993

Listeria ivanovii is capable of cell-to-cell spread involving actin polymerization.

I Karunasagar, G Krohne, W Goebel

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.8field-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

23 citing papers in PubMed, 64 citations in OpenAlex.

  1. Microorganisms · 2025
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  10. Actin-based motility of intracellular microbial pathogens.Microbiology and molecular biology reviews : MMBR · 2001
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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

3 authors at 1 institution in 1 country.

I KarunasagarLehrstuhl Mikrobiologie, Theodor Boveri-Institut für Biowissenschaften, Würzburg, Germany.
G Krohne
W Goebel
Würzburg Institute for Traffic Sciences (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Listeria ivanovii has been considered to be pathogenic to animals but has rarely been found associated with human infections. It has been claimed that L. ivanovii lacks the actA gene, which in L. monocytogenes encodes a protein required for interaction with host cell actin. Using fluorescence microscopy and electron microscopy, we demonstrate that L. ivanovii can invade mammalian cells, lyse the phagosomal membrane, polymerize host cell actin, reorganize actin to form tails, and spread from cell to cell. However, no DNA homologous to the actA gene could be detected by polymerase chain reaction. Further, L. ivanovii lacks the 90-kDa surface protein which in L. monocytogenes is encoded by actA. Despite the ability to spread from cell to cell, L. ivanovii differed significantly from L. monocytogenes in being unable to form plaques on monolayers of 3T3 fibroblast cells.

Indexed as

ActinsBacterial ProteinsBase SequenceCells, CulturedListeriaListeriosisMembrane ProteinsMicrofilament ProteinsMicroscopy, ElectronMicroscopy, FluorescenceMolecular Sequence DataPolymerase Chain ReactionTime FactorsViral Plaque AssayVirulenceactA protein, Listeria monocytogenesActinsBacterial ProteinsMembrane ProteinsMicrofilament Proteins

Identifiers

PMID8418038
PMCPMC302701
OpenAlexW1480981774

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.