Evidence map›Paper›PMID 42291191›Full record

ArticleiScience2026

Neuronal responses to cytokines limit intestinal hypermotility and systemic effects of colonic inflammation.

Jisun Jung, Alec Wehmeier, Zili Xie, David Horton, Emilie V Russler-Germain, Ellen Merrick Schill, Mark J Miller, Jonathan R Brestoff, Rodney Newberry, Brian S Kim and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Jisun JungDepartment of Internal Medicine, Division of Rheumatology, Washington University School of Medicine, St. Louis, MO, USA.
Alec WehmeierDepartment of Internal Medicine, Division of Rheumatology, Washington University School of Medicine, St. Louis, MO, USA.
Zili XieDepartment of Anesthesiology, The Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, USA.
David HortonDepartment of Internal Medicine, Division of Rheumatology, Washington University School of Medicine, St. Louis, MO, USA.
Emilie V Russler-GermainDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, USA.
Ellen Merrick SchillDepartment of Internal Medicine, Division of Gastroenterology, Washington University School of Medicine, St. Louis, MO, USA.
Mark J MillerDepartment of Medicine, Washington University in St. Louis, St. Louis, MO, USA.
Jonathan R BrestoffDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, USA.
Rodney NewberryDepartment of Internal Medicine, Division of Gastroenterology, Washington University School of Medicine, St. Louis, MO, USA.
Brian S KimDepartment of Anesthesiology, The Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, USA.
Hongzhen HuDepartment of Anesthesiology, The Center for the Study of Itch, Washington University School of Medicine, St. Louis, MO, USA.
Chyi-Song HsiehDepartment of Internal Medicine, Division of Rheumatology, Washington University School of Medicine, St. Louis, MO, USA.

Funding

Child Health Research CenterK12HD076224 · NICHD · WASHINGTON UNIVERSITY · PI MARK E. LOWE · 2013 to 2026
$6.2M
NICHD NIH HHS K12 HD076224
6 · The paper itself

Abstract

Inflammation results in increased gastrointestinal (GI) motility and diarrhea, but the mechanism remains unclear. Contrary to expectations, we found that neuronal responses to cytokine inhibited GI motility, as Nav1.8-Cre-mediated neuronal deletion of Jak1, a cytokine signaling intermediate, markedly increased GI motility at homeostasis. These cytokine-responsive neurons may reside in the enteric nervous system (ENS) based on the pattern of gene-deletion and GI motility induced by Nav1.8- and Trpv1-Cre. Cytokine receptors upstream of Jak1 that inhibit GI motility at homeostasis include IFNγ and IL-10, but not IL-4 or IFNα. While deficiency in cytokine inhibition of GI motility did not appear to affect the health of the mice at homeostasis, worse outcomes were observed after experimental Dextran sulfate sodium (DSS) colitis. Thus, we speculate that IFNγ and IL-10, cytokines associated with type 1 immune responses, may participate in a protective neuro-immune negative feedback loop to limit excessive GI motility during intestinal inflammation.

Indexed as

Cellular neuroscienceComponents of the immune systemMolecular biology

Identifiers

PMID42291191
PMCPMC13264127

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.