ArticleGut2006
Immune control of food intake: enteroendocrine cells are regulated by CD4+ T lymphocytes during small intestinal inflammation.
Article in Gut, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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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.
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.
Who cites it
34 citing papers in PubMed, 89 citations in OpenAlex.
- Fasting and nutrient-stimulated plasma peptide-YY levels are elevated in critical illness and associated with feed intolerance: an observational, controlled study.Critical care (London, England) · 2006Trial
- Review
- Guardians of the gut: influence of the enteric nervous system on the intestinal epithelial barrier.Frontiers in medicine · 2023Review
- Interactions between central nervous system and peripheral metabolic organs.Science China. Life sciences · 2022Review
- "Every cell is an immune cell; contributions of non-hematopoietic cells to anti-helminth immunity".Mucosal immunology · 2022Review
- The Gut-Brain Axis and Its Role in Controlling Eating Behavior in Intestinal Inflammation.Nutrients · 2021Review
- IL-25 Treatment Improves Metabolic Syndrome in High-Fat Diet and Genetic Models of Obesity.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- Maternal Microbiota Transfer Programs Offspring Eating Behavior.Frontiers in microbiology · 2021Article
- Helminth Sensing at the Intestinal Epithelial Barrier-A Taste of Things to Come.Frontiers in immunology · 2020Review
- IL-13-induced intestinal secretory epithelial cell antigen passages are required for IgE-mediated food-induced anaphylaxis.The Journal of allergy and clinical immunology · 2019Article
- GI inflammation Increases Sodium-Glucose Cotransporter Sglt1.International journal of molecular sciences · 2019Article
- Dietary supplementation with free methionine or methionine dipeptide mitigates intestinal oxidative stress induced byJournal of animal science and biotechnology · 2019Article
- First Responders: Innate Immunity to Helminths.Trends in parasitology · 2018Review
- Cholecystokinin octapeptide inhibits the inflammatory response and improves neurological outcome in a porcine model of cardiopulmonary resuscitation.Experimental and therapeutic medicine · 2018Article
- Anxiety, Depression, and the Microbiome: A Role for Gut Peptides.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Review
- Enteroendocrine cells-sensory sentinels of the intestinal environment and orchestrators of mucosal immunity.Mucosal immunology · 2018Review
- Review
- Parasites, nutrition, immune responses and biology of metabolic tissues.Parasite immunology · 2017Review
- Expression and Regulation of Cholecystokinin Receptor in the Chicken's Immune Organs and Cells.Journal of clinical & cellular immunology · 2016Article
- Regulation of energy balance by a gut-brain axis and involvement of the gut microbiota.Cellular and molecular life sciences : CMLS · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND AND
aimsGastrointestinal inflammation reduces food intake but the biological mechanisms explaining suppressed feeding during inflammation are unknown. We have used a model of upper gut infection (Trichinella spiralis in the mouse) to study the effect of inflammation on food intake, and explored the role of a key enteroendocrine cell (EEC) in the regulation of feeding by the immune response.
methodsFood intake of NIH mice infected with the intestinal nematode Trichinella spiralis was measured. Duodenal cholecystokinin (CCK) cells were counted. Plasma CCK was measured. Infected mice were treated with a specific CCK1 receptor antagonist, and food intake reassessed. The influence of the immune response on food intake and CCK was mechanistically examined by treating mice with CD4 or mast cell neutralising antibodies. The role of the T helper 2 response was further explored in mice genetically deficient for interleukin (IL)-4, IL-13, or IL-4Ralpha (receptor alpha subunit).
resultsFood intake of infected mice was significantly reduced at the temporal peak of intestinal inflammation. CCK expressing EEC were upregulated in infected mice, and plasma CCK levels were increased. A CCK1 receptor antagonist restored the food intake of infected mice to a significant degree. Furthermore, suppression of food intake was completely abolished in the absence of CD4+ T lymphocytes or IL-4Ralpha.
conclusionsThe data show for the first time that intestinal inflammation results in reduced food intake due to upregulation of CCK. Moreover, following infection, food intake and CCK expressing cells are under the specific control of CD4+ T-cells, via release of IL-4 and IL-13.
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What OpenQuestion holds
Registered trials
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.