Evidence map›Paper›PMID 39378308›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2025

Calcitonin gene-related peptide promotes epithelial reparative and anticolitic functions of IL-4 educated human macrophages.

Blanca E Callejas, James A Sousa, Kyle L Flannigan, Arthur Wang, Eve Higgins, Aydin I Herik, Shuhua Li, Sruthi Rajeev, Ryan Rosentreter, Remo Panaccione and 1 more

Abstract read
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In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 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
  2. Review
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Blanca E CallejasGastrointestinal Research Group, Inflammation Research Network and Host-Parasite Interactions Group, Department of Physiology and Pharmacology, Calvin, Phoebe and Joan Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
James A SousaGastrointestinal Research Group, Inflammation Research Network and Host-Parasite Interactions Group, Department of Physiology and Pharmacology, Calvin, Phoebe and Joan Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Kyle L FlanniganGastrointestinal Research Group, Inflammation Research Network and Host-Parasite Interactions Group, Department of Physiology and Pharmacology, Calvin, Phoebe and Joan Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Arthur WangGastrointestinal Research Group, Inflammation Research Network and Host-Parasite Interactions Group, Department of Physiology and Pharmacology, Calvin, Phoebe and Joan Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.ORCID 0009-0004-8207-6785
Eve HigginsGastrointestinal Research Group, Inflammation Research Network and Host-Parasite Interactions Group, Department of Physiology and Pharmacology, Calvin, Phoebe and Joan Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Aydin I HerikGastrointestinal Research Group, Inflammation Research Network and Host-Parasite Interactions Group, Department of Physiology and Pharmacology, Calvin, Phoebe and Joan Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.ORCID 0009-0009-5972-6192
Shuhua LiGastrointestinal Research Group, Inflammation Research Network and Host-Parasite Interactions Group, Department of Physiology and Pharmacology, Calvin, Phoebe and Joan Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Sruthi RajeevGastrointestinal Research Group, Inflammation Research Network and Host-Parasite Interactions Group, Department of Physiology and Pharmacology, Calvin, Phoebe and Joan Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.ORCID 0000-0002-5735-7479
Ryan RosentreterDivision of Gastroenterology and Hepatology, Gastrointestinal Research Group, Department of Medicine, Calvin, Phoebe, and Joan Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Remo PanaccioneDivision of Gastroenterology and Hepatology, Gastrointestinal Research Group, Department of Medicine, Calvin, Phoebe, and Joan Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Derek M McKayGastrointestinal Research Group, Inflammation Research Network and Host-Parasite Interactions Group, Department of Physiology and Pharmacology, Calvin, Phoebe and Joan Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.ORCID 0000-0002-0557-8210

Funding

Leona M. and Harry B. Helmsley Charitable Trust (Helmsley Charitable Trust) 2102-04983
6 · The paper itself

Abstract

Interleukin-4 activated human macrophages [M(IL4)s] promote epithelial wound healing and exert an anticolitic effect in a murine model. Blood monocyte-derived M(IL4)s from healthy donors and individuals with Crohn's disease had increased mRNA expression of the calcitonin gene-related peptide (CGRP) receptor chain, receptor activity modifying protein-1 (RAMP1), raising the issue of neural modulation of the M(IL4)s reparative function. Thus, human M(IL4)s were treated with CGRP and the cells' phagocytotic, epithelial wound repair and anticolitic functions were assessed. Initial studies confirmed upregulation of expression of the CGRP receptor, which was localized to the cell surface and was functional as determined by CGRP-evoked increases in cAMP. M(IL4,CGRP)s had increased mannose receptor (CD206) and FcγRIIa (CD32a) mRNA expression, a subtle, but significant, increase in phagocytosis and decreased chemokine production following the exposure to

Indexed as

Calcitonin Gene-Related PeptideInterleukin-4MacrophagesWound HealingAnimalsCaco-2 CellsCrohn DiseaseHomeodomain ProteinsHumansIntestinal MucosaLectins, C-TypeMiceMice, KnockoutPhagocytosisReceptors, Calcitonin Gene-Related PeptideCalcitonin Gene-Related PeptideHomeodomain ProteinsInterleukin-4Lectins, C-TypeRAG-1 proteinReceptors, Calcitonin Gene-Related PeptideCGRPIBDimmunotherapyM(IL4)neuroimmune interactionwound healing

Identifiers

PMID39378308

What OpenQuestion holds

Textmetadata
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.