Evidence map›Paper›PMID 38834738›Full record

ArticleScientific reports2024

Transcriptional profiling links unique human macrophage phenotypes to the growth of intracellular Salmonella enterica serovar Typhi.

Ruth Schade, Daniel S C Butler, Joy A McKenna, Blanda Di Luccia, Vida Shokoohi, Meagan Hamblin, Trung H M Pham, Denise M Monack

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. 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
  2. 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

8 authors.

Ruth SchadeDepartment of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA, 94305, USA.
Daniel S C Butler *Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA, 94305, USA.
Joy A McKenna *Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA, 94305, USA.
Blanda Di LucciaDepartment of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA, 94305, USA.
Vida ShokoohiStanford Functional Genomics Facility, Stanford University, Stanford, CA, USA.
Meagan HamblinDepartment of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA, 94305, USA.
Trung H M PhamDepartment of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA.
Denise M MonackDepartment of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA, 94305, USA. dmonack@stanford.edu.

Funding

Mechanisms of persistent Salmonella infectionR01AI116059 · NIAID · STANFORD UNIVERSITY · PI MONACK, DENISE M · 2015 to 2025
$4.6M
Dissecting Mechanisms of Granuloma Macrophage Polarization and Granuloma Formation in Chronic Salmonella InfectionK08AI143796 · NIAID · STANFORD UNIVERSITY · PI PHAM, TRUNG HOANG MINH · 2019 to 2023
$971k
National Institute of Allergy and Infectious Diseases K08-AI143796National Institute of Allergy and Infectious Diseases R01-AI116059NIAID NIH HHS K08 AI143796NIAID NIH HHS R01 AI116059Svenska Sällskapet för Medicinsk Forskning PD21-0150
6 · The paper itself

Abstract

Macrophages provide a crucial environment for Salmonella enterica serovar Typhi (S. Typhi) to multiply during typhoid fever, yet our understanding of how human macrophages and S. Typhi interact remains limited. In this study, we delve into the dynamics of S. Typhi replication within human macrophages and the resulting heterogeneous transcriptomic responses of macrophages during infection. Our study reveals key factors that influence macrophage diversity, uncovering distinct immune and metabolic pathways associated with different stages of S. Typhi intracellular replication in macrophages. Of note, we found that macrophages harboring replicating S. Typhi are skewed towards an M1 pro-inflammatory state, whereas macrophages containing non-replicating S. Typhi exhibit neither a distinct M1 pro-inflammatory nor M2 anti-inflammatory state. Additionally, macrophages with replicating S. Typhi were characterized by the increased expression of genes associated with STAT3 phosphorylation and the activation of the STAT3 transcription factor. Our results shed light on transcriptomic pathways involved in the susceptibility of human macrophages to intracellular S. Typhi replication, thereby providing crucial insight into host phenotypes that restrict and support S. Typhi infection.

Indexed as

MacrophagesSalmonella typhiSTAT3 Transcription FactorTyphoid FeverGene Expression ProfilingHumansPhenotypePhosphorylationTranscriptomeSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID38834738
PMCPMC11150401

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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.