Evidence map›Paper›PMID 26414184›Full record

ArticlePloS one2015

The Viral Mimetic Polyinosinic:Polycytidylic Acid Alters the Growth Characteristics of Small Intestinal and Colonic Crypt Cultures.

Julie M Davies, Rebeca Santaolalla, Richard J von Furstenberg, Susan J Henning, Maria T Abreu

Abstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

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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

5 authors.

Julie M DaviesMiller School of Medicine, Division of Gastroenterology, University of Miami, Miami, Florida, United States of America.
Rebeca SantaolallaMiller School of Medicine, Division of Gastroenterology, University of Miami, Miami, Florida, United States of America.
Richard J von FurstenbergDepartment of Medicine and Cell Biology and Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
Susan J HenningDepartment of Medicine and Cell Biology and Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
Maria T AbreuMiller School of Medicine, Division of Gastroenterology, University of Miami, Miami, Florida, United States of America.

Funding

Role of TLR4 in Colitis Associated NeoplasiaR01DK099076 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Maria Teresa Abreu · 2014 to 2026
$4.7M
Role of TLR4 in colitis-associated neoplasiaR01CA137869 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI ABREU, MARIA TERESA · 2009 to 2013
$1.5M
NCI NIH HHS 5R01CA137869-05NCI NIH HHS R01 CA137869NIDDK NIH HHS 2R01DK099076-06A1NIDDK NIH HHS R01 DK099076
6 · The paper itself

Abstract

BACKGROUND &

aimsThe intestinal epithelium is the first line of defense against enteric pathogens. We investigated the response of small intestinal and colonic crypt cultures to a panel of toll-like receptor ligands to assess the impact of microbial pattern recognition on epithelial growth.

methodsPrimary murine jejunal enteroids and colonoids were cultured with lipopeptide Pam3CSK4, lipopolysaccharide (LPS) or polyinosinic:polycytidylic acid (Poly I:C) for 4 to 6 days. Surface area, budding and survival were assessed. Proliferation and numbers of lysozyme positive cells were quantified by flow cytometry. Gene expression was assessed by Nanostring and qRT-PCR.

resultsExposure to Pam3CSK4 and LPS had minimal impact on either enteroids or colonoids. In contrast, Poly I:C increased the surface area of enteroids, while colonoids demonstrated decreased budding. Survival was decreased by Poly I:C in enteroids but not in colonoids. Both enteroids and colonoids exhibited upregulated gene expression of chemokines, but these were increased in magnitude in enteroids. Decreases in gene expression associated with epithelial differentiation and lysozyme positive cells were more apparent in enteroids than in colonoids. Baseline gene expression between enteroids and colonoids differed markedly in levels of stem cell and inflammatory markers. The changes in morphology induced by Poly I:C were mediated by the toll-like receptor adaptor molecule 1 (Ticam1) in enteroids but not in colonoids.

conclusionsPoly I:C alters the molecular program of epithelial cells and shifts from absorption and digestion towards defense and inflammation. Diversity of responses to microbial patterns in enteroids and colonoids may underlie differences in susceptibility to infection along the intestinal tract.

Indexed as

Adaptor Proteins, Vesicular TransportAnimalsBiomarkersCell CountCell ProliferationCells, CulturedCell ShapeCell SurvivalColonDown-RegulationIntestine, SmallJejunumMice, Inbred C57BLMuramidaseOrganoidsPoly I-CAdaptor Proteins, Vesicular TransportBiomarkersMuramidasePoly I-CRNA, Double-Stranded

Identifiers

PMID26414184
PMCPMC4587363

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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.