Evidence map›Paper›PMID 21822909›Full record

ArticleDigestive diseases and sciences2012

Increased bacterial translocation in gluten-sensitive mice is independent of small intestinal paracellular permeability defect.

Manuel A Silva, Jennifer Jury, Yolanda Sanz, Michelle Wiepjes, Xianxi Huang, Joseph A Murray, Chella S David, Alessio Fasano, Elena F Verdú

Open access · greenAbstract read
In one paragraph

Article in Digestive diseases and sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Toll-like Receptors and Celiac Disease.International journal of molecular sciences · 2022
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Latest in vitro and in vivo models of celiac disease.Expert opinion on drug discovery · 2013
    Review
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 7 institutions in 4 countries.

Manuel A SilvaDepartment of Medicine, Health Sciences Centre, Farncombe Family Digestive Health Research Institute, McMaster University, 1200 Main Street West, Hamilton, ON L8N 3Z5, Canada. msilvamu@hotmail.com
Jennifer Jury
Yolanda Sanz
Michelle Wiepjes
Xianxi Huang
Joseph A Murray
Chella S David
Alessio Fasano
Elena F Verdú
Health Sciences Centre · CAConsejo Superior de Investigaciones Científicas · ESMayo Clinic · USMcMaster University · CAPopulation Health Research Institute · CAUniversity of Maryland, Baltimore · USWinnMed · US

Funding

Zot, Zonulin, and Pathophysiology of Intestinal Tight JunctionsR01DK048373 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI FASANO, ALESSIO · 1996 to 2015
$4.4M
A HLA Mouse Model for Gluten Sensitivity and EnteropathyR01DK071003 · NIDDK · MAYO CLINIC ROCHESTER · PI MURRAY, JOSEPH A · 2006 to 2009
$1.1M
CIHR GN2-114709NIDDK NIH HHS R01 DK048373NIDDK NIH HHS R01 DK048373-13NIDDK NIH HHS R01 DK071003NIDDK NIH HHS R01 DK71003
6 · The paper itself

Abstract

aimWe investigated whether treatment with gliadin induces a paracellular permeability defect that enhances bacterial translocation to mesenteric lymph nodes (MLN) via resident dendritic cells (DC) expressing TLR-2 or 4 in HCD4/HLA-DQ8 transgenic mice.

methodsHLA-DQ8 transgenic mice were sensitized and subsequently gavaged with gliadin, in the presence or absence of AT1001 (paracellular permeability inhibitor). Non-sensitized mice were gavaged with indomethacin (permeability inducer) or rice cereal. CD11c and CD103 (DC markers) and TLR-2 and 4 were investigated by immunostaining. Intestinal permeability was assessed by paracellular flux of (51)Cr-EDTA in Ussing chambers. Bacterial translocation to MLN was performed by plate counting on aerobic and anaerobic conditions.

resultsIn gliadin-treated mice, both (51)Cr-EDTA flux in jejunal mucosa and aerobic and anaerobic bacterial counts in MLN were increased (p < 0.05) compared to indomethacin-treated mice and controls. The inhibitor AT1001 normalized (51)Cr-EDTA flux, but had no effect on bacterial translocation in gliadin-treated mice. In addition, changes in mucosal DC marker distribution such as increased (p < 0.05) trans-epithelial CD103(+) cells and reduction (p < 0.05) of CD11c immunostaining were detected in gliadin-treated mice. Moreover, changes in DC markers and TLR-2 or 4 immunophenotypes were not associated.

conclusionsPharmacological restoration of paracellular permeability was not sufficient to prevent bacterial translocation in gluten-sensitive mice. We hypothesize that transcellular mechanisms involving CD103(+)DC and CD11c(+)DC may explain in gluten-sensitive HCD4/HLA-DQ8 transgenic mice the sustained increased bacterial translocation observed in the absence of a significant inflammatory response.

Indexed as

AnimalsAntigens, CDBacterial TranslocationCD11c AntigenCeliac DiseaseCell Membrane PermeabilityDendritic CellsDisease Models, AnimalGliadinHLA-DQ AntigensIntegrin alpha ChainsIntestine, SmallLymph NodesMaleMiceMice, Transgenicalpha E integrinsAntigens, CDCD11c AntigenGliadinHLA-DQ8 antigenHLA-DQ AntigensIntegrin alpha Chainslarazotide acetateOligopeptidesTlr2 protein, mouseTlr4 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID21822909
PMCPMC3507358
OpenAlexW1997647948

What OpenQuestion holds

Textmetadata
LicenceTDM
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.