Evidence map›Paper›PMID 27760340›Full record

ArticleImmunity2016

Macrophage Epithelial Reprogramming Underlies Mycobacterial Granuloma Formation and Promotes Infection.

Mark R Cronan, Rebecca W Beerman, Allison F Rosenberg, Joseph W Saelens, Matthew G Johnson, Stefan H Oehlers, Dana M Sisk, Kristen L Jurcic Smith, Neil A Medvitz, Sara E Miller and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed
12.6field-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

140 citing papers in PubMed, 241 citations in OpenAlex.

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  19. A granulin-positive macrophage subtype in mycobacterial granulomas alleviates tissue damage by limiting excessive inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  20. Article

80 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 3 institutions in 1 country.

Mark R CronanDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.
Rebecca W BeermanDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.
Allison F RosenbergDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.
Joseph W SaelensDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.
Matthew G JohnsonDivision of Infectious Diseases, Duke University School of Medicine, Durham, NC 27710, USA; Department of Medicine, Duke University School of Medicine, Durham, NC 27710, USA.
Stefan H OehlersDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.
Dana M SiskDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.
Kristen L Jurcic SmithDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA; Department of Medicine, Duke University School of Medicine, Durham, NC 27710, USA.
Neil A MedvitzDepartment of Pathology, Duke University School of Medicine, Durham, NC 27710, USA.
Sara E MillerDepartment of Pathology, Duke University School of Medicine, Durham, NC 27710, USA.
Le A TrinhMolecular and Computational Biology and Translational Imaging Center, University of Southern California, Los Angeles, CA 90089, USA.
Scott E FraserMolecular and Computational Biology and Translational Imaging Center, University of Southern California, Los Angeles, CA 90089, USA.
John F MaddenDepartment of Pathology, Duke University School of Medicine, Durham, NC 27710, USA.
Joanne TurnerDepartment of Microbial Infection and Immunity, The Ohio State University, Columbus, OH 43210, USA; Center for Microbial Interface Biology, The Ohio State University, Columbus, OH 43210, USA.
Jason E StoutDivision of Infectious Diseases, Duke University School of Medicine, Durham, NC 27710, USA; Department of Medicine, Duke University School of Medicine, Durham, NC 27710, USA.
Sunhee LeeDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA; Department of Medicine, Duke University School of Medicine, Durham, NC 27710, USA.
David M TobinDepartment of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA; Department of Immunology, Duke University School of Medicine, Durham, NC 27710, USA. Electronic address: david.tobin@duke.edu.
Duke University · USImaging Center · USInterface (United States) · US

Funding

Social and Behavioral Sciences CoreP30AI064518 · NIAID · DUKE UNIVERSITY · PI Susanna Naggie, GEORGIA Doris TOMARAS · 2005 to 2026
$50.5M
Ruth L. Kirschstein National Research Service Award (NRSA)- T32T32AI007392 · NIAID · DUKE UNIVERSITY · PI Amy Lynn Corneli, Guido Ferrari · 1990 to 2026
$9.8M
TRAINING PROGRAM IN INFLAMMATORY AND IMMUNOLOGICALT32AI007217 · NIAID · DUKE UNIVERSITY · PI PISETSKY, DAVID STEPHEN · 1985 to 2015
$3.3M
Modulating Eicosanoids to Treat Tuberculosis: Personalized, Host-directed TherapyDP2OD008614 · OD · DUKE UNIVERSITY · PI TOBIN, DAVID M. · 2011 to 2011
$2.4M
The Genetic Basis of Bone Disease in Mycobacterial InfectionR21AI111067 · NIAID · DUKE UNIVERSITY · PI LEE, SUNHEE, STOUT, JASON E · 2015 to 2016
$434k
NIAID NIH HHS P30 AI064518NIAID NIH HHS R21 AI111067NIAID NIH HHS T32 AI007217NIAID NIH HHS T32 AI007392NIH HHS DP2 OD008614
6 · The paper itself

Abstract

Mycobacterium tuberculosis infection in humans triggers formation of granulomas, which are tightly organized immune cell aggregates that are the central structure of tuberculosis. Infected and uninfected macrophages interdigitate, assuming an altered, flattened appearance. Although pathologists have described these changes for over a century, the molecular and cellular programs underlying this transition are unclear. Here, using the zebrafish-Mycobacterium marinum model, we found that mycobacterial granuloma formation is accompanied by macrophage induction of canonical epithelial molecules and structures. We identified fundamental macrophage reprogramming events that parallel E-cadherin-dependent mesenchymal-epithelial transitions. Macrophage-specific disruption of E-cadherin function resulted in disordered granuloma formation, enhanced immune cell access, decreased bacterial burden, and increased host survival, suggesting that the granuloma can also serve a bacteria-protective role. Granuloma macrophages in humans with tuberculosis were similarly transformed. Thus, during mycobacterial infection, granuloma macrophages are broadly reprogrammed by epithelial modules, and this reprogramming alters the trajectory of infection and the associated immune response.

Indexed as

AnimalsCadherinsEpitheliumGranulomaMacrophagesMycobacterium marinumMycobacterium tuberculosisZebrafishCadherins

Identifiers

PMID27760340
PMCPMC5268069
OpenAlexW2532005031

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.