Evidence map›Paper›PMID 26668389›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Contributions of microbiome and mechanical deformation to intestinal bacterial overgrowth and inflammation in a human gut-on-a-chip.

Hyun Jung Kim, Hu Li, James J Collins, Donald E Ingber

Open access · bronzeAbstract readEvaluation Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 486 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
486citing papers in PubMed, 1 pooled it
28.8field-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

486 citing papers in PubMed, 1 synthesis or guideline pooled it, 891 citations in OpenAlex.

  1. Pooled it
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  17. Live and heat-treatediScience · 2026
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426 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

4 authors at 1 institution in 1 country.

Hyun Jung KimWyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA 02115;
Hu LiWyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA 02115;
James J CollinsWyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA 02115; Institute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02139; Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139; Synthetic Biology Center, Massachusetts Institute of Technology, Cambridge, MA 02139; Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, MA 02142; Harvard-Massachusetts Institute of Technology Program in Health Sciences and Technology, Cambridge, MA 02139; jimjc@mit.edu don.ingber@wyss.harvard.edu.
Donald E IngberWyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA 02115; Vascular Biology Program, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115; Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, MA 02138 jimjc@mit.edu don.ingber@wyss.harvard.edu.
Harvard University · US

Funding

FDA HHS HHSF223201310079C
6 · The paper itself

Abstract

A human gut-on-a-chip microdevice was used to coculture multiple commensal microbes in contact with living human intestinal epithelial cells for more than a week in vitro and to analyze how gut microbiome, inflammatory cells, and peristalsis-associated mechanical deformations independently contribute to intestinal bacterial overgrowth and inflammation. This in vitro model replicated results from past animal and human studies, including demonstration that probiotic and antibiotic therapies can suppress villus injury induced by pathogenic bacteria. By ceasing peristalsis-like motions while maintaining luminal flow, lack of epithelial deformation was shown to trigger bacterial overgrowth similar to that observed in patients with ileus and inflammatory bowel disease. Analysis of intestinal inflammation on-chip revealed that immune cells and lipopolysaccharide endotoxin together stimulate epithelial cells to produce four proinflammatory cytokines (IL-8, IL-6, IL-1β, and TNF-α) that are necessary and sufficient to induce villus injury and compromise intestinal barrier function. Thus, this human gut-on-a-chip can be used to analyze contributions of microbiome to intestinal pathophysiology and dissect disease mechanisms in a controlled manner that is not possible using existing in vitro systems or animal models.

Indexed as

Lab-On-A-Chip DevicesModels, BiologicalAnimalsAnti-Bacterial AgentsBacteriaCaco-2 CellsHumansIleusInflammatory Bowel DiseasesInterleukin-1betaInterleukin-6Interleukin-8Intestinal MucosaIn Vitro TechniquesMicrobiotaPeristalsisAnti-Bacterial AgentsInterleukin-1betaInterleukin-6Interleukin-8Tumor Necrosis Factor-alphagut-on-a-chipinflammatory bowel diseaseintestinemechanicalmicrobiome

Identifiers

PMID26668389
PMCPMC4711860
OpenAlexW2214747519

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.