Evidence map›Paper›PMID 39368481›Full record

ArticleCell reports. Medicine2024

The sympathetic nervous system drives hyperinflammatory responses to Clostridioides difficile infection.

David Tyus, Jhansi L Leslie, Farha Naz, Md Jashim Uddin, Brandon Thompson, William A Petri

Abstract read
In one paragraph

Article in Cell reports. Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Sympathetic regulation of the host immune response to bacterial sepsis.Clinical science (London, England : 1979) · 2025
    Review
  5. Review
  6. Review
  7. Article
  8. Article
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

6 authors.

David TyusNeuroscience Graduate Program, University of Virginia Health System, Charlottesville, VA 22908, USA.
Jhansi L LeslieDivision of Infectious Disease and International Health, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.
Farha NazDivision of Infectious Disease and International Health, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.
Md Jashim UddinDivision of Infectious Disease and International Health, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.
Brandon ThompsonDepartments of Medicine, Pathology, Microbiology, Immunology and Cancer Biology, University of Virginia Health System, Charlottesville, VA 22908, USA; Division of Infectious Disease and International Health, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.
William A PetriNeuroscience Graduate Program, University of Virginia Health System, Charlottesville, VA 22908, USA; Departments of Medicine, Pathology, Microbiology, Immunology and Cancer Biology, University of Virginia Health System, Charlottesville, VA 22908, USA; Division of Infectious Disease and International Health, University of Virginia School of Medicine, Charlottesville, VA 22908, USA. Electronic address: wap3g@virginia.edu.

Funding

INFECTIOUS DISEASES TRAINING PROGRAMT32AI007046 · NIAID · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Alison K Criss, William A Petri · 1985 to 2026
$15.3M
Role of Th17 in Severe and Recurrent C. difficile InfectionR01AI152477 · NIAID · UNIVERSITY OF VIRGINIA · PI PETRI, WILLIAM A, RAMAKRISHNAN, GIRIJA · 2020 to 2025
$7.1M
Role of Type 2 Immunity in Innate Protection from C. difficileR01AI124214 · NIAID · UNIVERSITY OF VIRGINIA · PI William A Petri · 2016 to 2026
$5.4M
NIAID NIH HHS R01 AI124214NIAID NIH HHS R01 AI152477NIAID NIH HHS T32 AI007046
6 · The paper itself

Abstract

Clostridioides difficile infection (CDI) is a leading cause of hospital-acquired infections in the United States, known for triggering severe disease by hyperactivation of the host response. In this study, we determine the impact of the sympathetic nervous system (SNS) on CDI disease severity. Mouse models of CDI are administered inhibitors of SNS activity prior to CDI. Chemical sympathectomy or pharmacological inhibition of norepinephrine synthesis greatly reduces mortality and disease severity in the CDI model. Pharmacological blockade or genetic ablation of the alpha 2 adrenergic receptor ameliorates intestinal inflammation, disease severity, and mortality rate. These results underscore the role of the SNS and the alpha 2 adrenergic receptor in CDI pathogenesis and suggest that targeting neural systems could be a promising approach to therapy in severe disease.

Indexed as

Clostridioides difficileClostridium InfectionsNorepinephrineSympathetic Nervous SystemAnimalsDisease Models, AnimalInflammationMaleMiceMice, Inbred C57BLReceptors, Adrenergic, alpha-2NorepinephrineReceptors, Adrenergic, alpha-2adrenergic receptorsClostridioides difficilecolitisnorepinephrinesympathetic nervous system

Identifiers

PMID39368481
PMCPMC11513855

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.