Evidence map›Paper›PMID 39951038›Full record

ArticleInflammatory bowel diseases2025

Deep Sequencing of Crohn's Disease Lamina Propria Phagocytes Identifies Pathobionts and Correlates With Pro-Inflammatory Gene Expression.

Gillian E Jacobsen, Eddy E Gonzalez, Payton Mendygral, Katerina M Faust, Hajar Hazime, Irina Fernandez, Ana M Santander, Maria A Quintero, Chunsu Jiang, Oriana M Damas and 8 more

Abstract read
In one paragraph

Article in Inflammatory bowel diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
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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

18 authors.

Gillian E JacobsenDepartment of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL, USA.
Eddy E GonzalezDepartment of Medicine, Crohn's and Colitis Center, University of Miami Miller School of Medicine, Miami, FL, USA.
Payton MendygralDepartment of Medicine, Crohn's and Colitis Center, University of Miami Miller School of Medicine, Miami, FL, USA.
Katerina M FaustDepartment of Medicine, Crohn's and Colitis Center, University of Miami Miller School of Medicine, Miami, FL, USA.ORCID 0000-0002-7277-5505
Hajar HazimeDepartment of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL, USA.
Irina FernandezDepartment of Medicine, Crohn's and Colitis Center, University of Miami Miller School of Medicine, Miami, FL, USA.
Ana M SantanderDepartment of Medicine, Crohn's and Colitis Center, University of Miami Miller School of Medicine, Miami, FL, USA.
Maria A QuinteroDepartment of Medicine, Crohn's and Colitis Center, University of Miami Miller School of Medicine, Miami, FL, USA.
Chunsu JiangDepartment of Medicine, Crohn's and Colitis Center, University of Miami Miller School of Medicine, Miami, FL, USA.
Oriana M DamasDepartment of Medicine, Crohn's and Colitis Center, University of Miami Miller School of Medicine, Miami, FL, USA.
Amar R DeshpandeDepartment of Medicine, Crohn's and Colitis Center, University of Miami Miller School of Medicine, Miami, FL, USA.
David H KermanDepartment of Medicine, Crohn's and Colitis Center, University of Miami Miller School of Medicine, Miami, FL, USA.
Siobhan ProksellDepartment of Medicine, Crohn's and Colitis Center, University of Miami Miller School of Medicine, Miami, FL, USA.
Morgan Sendzischew ShaneDepartment of Medicine, Crohn's and Colitis Center, University of Miami Miller School of Medicine, Miami, FL, USA.
Daniel A SussmanDepartment of Medicine, Crohn's and Colitis Center, University of Miami Miller School of Medicine, Miami, FL, USA.
Bassel GhaddarCenter for Systems and Computational Biology, Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ, USA.
Trevor CickovskBioinformatics Research Group (BioRG), Knight Foundation School of Computing and Information Sciences, Florida International University, Miami, FL, USA.
Maria T AbreuDepartment of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL, USA.ORCID 0000-0002-7294-0574

Funding

Role of TLR4 in Colitis Associated NeoplasiaR01DK099076 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Maria Teresa Abreu · 2014 to 2026
$4.7M
Predoctoral Training in Translational ImmunologyT32AI162624 · NIAID · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Thomas R Malek · 2022 to 2026
$894k
National Institute of Allergy and Infectious Diseases T32AI162624NIAID NIH HHS T32 AI162624NIDDK NIH HHS R01 DK099076NIDDK NIH HHS R01DK099076
6 · The paper itself

Abstract

backgroundCrohn's disease (CD) is characterized by an inflammatory response to gut microbiota. Macrophages and dendritic cells play an active role in CD inflammation. Specific microbiota have been implicated in the pathogenesis of ileal CD. We investigated the phagocyte-associated microbiome using an unbiased sequencing approach to identify potential pathobionts and elucidate the host response to these microbes.

methodsWe collected ileal and colonic mucosal biopsies from CD patients and controls without inflammatory bowel disease (IBD), isolated lamina propria phagocytes (CD11b+ cells), and performed deep RNA sequencing (n = 37). Reads were mapped to the human genome for host gene expression analysis and a prokaryotic database for microbiome taxonomic and metatranscriptomic profiling. Results were confirmed in a second IBD cohort (n = 17). Lysed lamina propria cells were plated for bacterial culturing; isolated colonies underwent whole genome sequencing (n = 11).

resultsCrohn's disease ileal phagocytes contained higher relative abundances of Escherichia coli, Ruminococcus gnavus, and Enterocloster spp. than those from controls. CD phagocyte-associated microbes had increased expression of lipopolysaccharide (LPS) biosynthesis pathways. Phagocytes with a higher pathobiont burden showed increased expression of pro-inflammatory and antimicrobial genes, including PI3 (antimicrobial peptide) and BPIFB1 (LPS-binding molecule). E. coli isolated from the CD lamina propria had more flagellar motility and antibiotic resistance genes than control-derived strains.

conclusionsLamina propria resident phagocytes harbor bacterial strains that may act as pathobionts in CD. Our findings shed light on the role of pathobionts and the immune response in CD pathogenesis and suggest new targets for therapies.

Indexed as

Crohn DiseaseGastrointestinal MicrobiomeInflammationIntestinal MucosaPhagocytesAdultCase-Control StudiesEscherichia coliEubacterialesFemaleHigh-Throughput Nucleotide SequencingHumansIleumMaleMiddle AgedYoung Adultinflammatory bowel diseaselipopolysaccharidemetatranscriptomemicrobiome

Identifiers

PMID39951038
PMCPMC12069990

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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.