Evidence map›Paper›PMID 22534208›Full record

ArticleGut pathogens2012

Rapid paracellular transmigration of Campylobacter jejuni across polarized epithelial cells without affecting TER: role of proteolytic-active HtrA cleaving E-cadherin but not fibronectin.

Manja Boehm, Benjamin Hoy, Manfred Rohde, Nicole Tegtmeyer, Kristoffer T Bæk, Omar A Oyarzabal, Lone Brøndsted, Silja Wessler, Steffen Backert

Open access · goldAbstract read
In one paragraph

Article in Gut pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
16.7field-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

93 citing papers in PubMed, 142 citations in OpenAlex.

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33 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

9 authors at 4 institutions in 4 countries.

Manja Boehm *School for Medicine and Medical Science, University College Dublin, Belfield Campus, Dublin-4, Ireland.
Benjamin Hoy *The Division of Microbiology, University Salzburg, A-5020, Salzburg, Austria.
Manfred Rohde *The Department of Medical Microbiology, Helmholtz Center for Infection Research, Inhoffen Str. 7, D-38124, Braunschweig, Germany.
Nicole TegtmeyerSchool for Medicine and Medical Science, University College Dublin, Belfield Campus, Dublin-4, Ireland.
Kristoffer T BækThe Department of Veterinary Disease Biology, University Copenhagen, Stigbøjlen 4, DK-1870, Frederiksberg C, Denmark.
Omar A OyarzabalInstitute for Environmental Health, Inc., 15300 Bothell Way NE Lake Forest Park, Seattle, WA, 98155, USA.
Lone BrøndstedThe Department of Veterinary Disease Biology, University Copenhagen, Stigbøjlen 4, DK-1870, Frederiksberg C, Denmark.
Silja WesslerThe Division of Microbiology, University Salzburg, A-5020, Salzburg, Austria.
Steffen BackertSchool for Medicine and Medical Science, University College Dublin, Belfield Campus, Dublin-4, Ireland.
University College Dublin · IEUniversity of Copenhagen · DKUniversity of Salzburg · ATHelmholtz Centre for Infection Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCampylobacter jejuni is one of the most important bacterial pathogens causing food-borne illness worldwide. Crossing the intestinal epithelial barrier and host cell entry by C. jejuni is considered the primary reason of damage to the intestinal tissue, but the molecular mechanisms as well as major bacterial and host cell factors involved in this process are still widely unclear.

resultsIn the present study, we characterized the serine protease HtrA (high-temperature requirement A) of C. jejuni as a secreted virulence factor with important proteolytic functions. Infection studies and in vitro cleavage assays showed that C. jejuni's HtrA triggers shedding of the extracellular E-cadherin NTF domain (90 kDa) of non-polarised INT-407 and polarized MKN-28 epithelial cells, but fibronectin was not cleaved as seen for H. pylori's HtrA. Deletion of the htrA gene in C. jejuni or expression of a protease-deficient S197A point mutant did not lead to loss of flagella or reduced bacterial motility, but led to severe defects in E-cadherin cleavage and transmigration of the bacteria across polarized MKN-28 cell layers. Unlike other highly invasive pathogens, transmigration across polarized cells by wild-type C. jejuni is highly efficient and is achieved within a few minutes of infection. Interestingly, E-cadherin cleavage by C. jejuni occurs in a limited fashion and transmigration required the intact flagella as well as HtrA protease activity, but does not reduce transepithelial electrical resistance (TER) as seen with Salmonella, Shigella, Listeria or Neisseria.

conclusionThese results suggest that HtrA-mediated E-cadherin cleavage is involved in rapid crossing of the epithelial barrier by C. jejuni via a very specific mechanism using the paracellular route to reach basolateral surfaces, but does not cleave the fibronectin receptor which is necessary for cell entry.

Identifiers

PMID22534208
PMCPMC3413534
OpenAlexW2130610744

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Registered trials

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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.