Evidence map›Paper›PMID 33707230›Full record

ArticleGut2022

Novel pathomechanism for spontaneous bacterial peritonitis: disruption of cell junctions by cellular and bacterial proteases.

Marika Haderer, Philip Neubert, Eva Rinner, Annika Scholtis, Lucile Broncy, Heidi Gschwendtner, Arne Kandulski, Vlad Pavel, Alexander Mehrl, Christoph Brochhausen and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Gut, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 59 citations in OpenAlex.

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  16. IDCases · 2025
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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

14 authors at 1 institution in 1 country.

Marika HadererDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology, Rheumatology and Infectious diseases, University Hospital Regensburg, Regensburg, Bavaria, Germany.ORCID 0000-0002-2197-1944
Philip NeubertDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology, Rheumatology and Infectious diseases, University Hospital Regensburg, Regensburg, Bavaria, Germany.
Eva RinnerDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology, Rheumatology and Infectious diseases, University Hospital Regensburg, Regensburg, Bavaria, Germany.
Annika ScholtisDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology, Rheumatology and Infectious diseases, University Hospital Regensburg, Regensburg, Bavaria, Germany.
Lucile BroncyDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology, Rheumatology and Infectious diseases, University Hospital Regensburg, Regensburg, Bavaria, Germany.
Heidi GschwendtnerDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology, Rheumatology and Infectious diseases, University Hospital Regensburg, Regensburg, Bavaria, Germany.
Arne KandulskiDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology, Rheumatology and Infectious diseases, University Hospital Regensburg, Regensburg, Bavaria, Germany.
Vlad PavelDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology, Rheumatology and Infectious diseases, University Hospital Regensburg, Regensburg, Bavaria, Germany.
Alexander MehrlDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology, Rheumatology and Infectious diseases, University Hospital Regensburg, Regensburg, Bavaria, Germany.
Christoph BrochhausenDepartment of Pathology, University Hospital Regensburg, Regensburg, Bavaria, Germany.
Sophie SchlosserDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology, Rheumatology and Infectious diseases, University Hospital Regensburg, Regensburg, Bavaria, Germany.
Karsten GülowDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology, Rheumatology and Infectious diseases, University Hospital Regensburg, Regensburg, Bavaria, Germany.
Claudia KunstDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology, Rheumatology and Infectious diseases, University Hospital Regensburg, Regensburg, Bavaria, Germany.
Martina MüllerDepartment of Internal Medicine I, Gastroenterology, Hepatology, Endocrinology, Rheumatology and Infectious diseases, University Hospital Regensburg, Regensburg, Bavaria, Germany martina.mueller-schilling@ukr.de.
University Hospital Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveSpontaneous bacterial peritonitis (SBP) is a life-threatening complication of liver cirrhosis with a 1-year mortality of 66%. Bacterial translocation (BT) from the intestine to the mesenteric lymph nodes is crucial for the pathogenesis of SBP.

designSince BT presupposes a leaky intestinal epithelium, the integrity of mucus and epithelial cell junctions (E-cadherin and occludin) was examined in colonic biopsies from patients with liver cirrhosis and controls. SBP-inducing

resultsSBP-derived

conclusionPatients with liver cirrhosis show a reduced thickness of colonic mucus, which allows bacteria-to-epithelial cell contact. Intestinal bacteria induce degradation of occludin by exploiting the proteasome of epithelial cells. We identified a novel bacterial protease activity of patient-derived SBP-inducing bacteria, which is responsible for the cleavage of E-cadherin structures. Inhibition of this protease activity leads to stabilisation of cell junctions. Thus, targeting these mechanisms by blocking the ubiquitin-proteasome system and/or the bacterial protease activity might interfere with BT and constitute a novel innovative therapeutic strategy to prevent SBP in patients with liver cirrhosis.

Indexed as

AscitesBacterial TranslocationCaco-2 CellsCadherinsCase-Control StudiesCoculture TechniquesColonEscherichia coliFemaleHumansIntercellular JunctionsLiver CirrhosisMaleOccludinPeptide HydrolasesPeritonitisCadherinsOccludinPeptide Hydrolasesbacterial translocationE. coliliver cirrhosisperitonitis

Identifiers

PMID33707230
PMCPMC8862089
OpenAlexW3135871346

What OpenQuestion holds

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LicenceCC BY-NC
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.