ArticleGastroenterology2018
Change in Populations of Macrophages Promotes Development of Delayed Gastric Emptying in Mice.
Article in Gastroenterology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Spectrum of Interstitial Cell of Cajal Deficits in Chronic Gastroduodenal Disorders: Systematic Review and Meta-Analysis.The American journal of gastroenterology · 2026Pooled it
- Phenotypic switching of gastrointestinal smooth muscle cells and the regulatory role of macrophages: a literature review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Muscularis EGR1 Deficiency Impairs M2 Macrophage Polarization and Disrupts Gastric Motility in Diabetic Gastroparesis.Neurogastroenterology and motility · 2026Article
- Advances in Understanding Calcium Sensitization in Gastrointestinal Smooth Muscles: Pathways, Interstitial Cells, and Disease.Journal of neurogastroenterology and motility · 2026Review
- Changes in interstitial cells of Cajal calcium activity in a diabetic mouse model of delayed gastric emptying.The Journal of physiology · 2026Article
- Review
- Macrophages dynamically integrate neuro-immune-microbial network signals: their role in gastrointestinal motility disorders and targeting potential.Frontiers in immunology · 2026Review
- Heterogeneity of Muscularis Macrophages in the Stomach.Gastro hep advances · 2026Article
- Intestinal neuron-associated macrophages in health and disease.Nature immunology · 2025Review
- Gastroparesis, a diabetic complication causing further, even serious, complications: How to prevent its worsening?World journal of gastroenterology · 2025Article
- Mass cytometric analysis of circulating monocyte subsets in a murine model of diabetic gastroparesis.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Pharmacologic treatments for gastroparesis.Pharmacological reviews · 2025Review
- In Vitro Antiviral Activity of a Silydianin-Rich Extract fromAntibiotics (Basel, Switzerland) · 2025Article
- Microbiota and enteric nervous system crosstalk in diabetic gastroenteropathy: bridging mechanistic insights to microbiome-based therapies.Frontiers in cellular and infection microbiology · 2025Review
- Emerging roles of traditional Chinese medicine in the treatment of diabetic gastroparesis.Frontiers in nutrition · 2025Review
- Neuroimmune Crossroads: The Interplay of the Enteric Nervous System and Intestinal Macrophages in Gut Homeostasis and Disease.Biomolecules · 2024Review
- Article
- Neuroimmunophysiology of the gastrointestinal tract.American journal of physiology. Gastrointestinal and liver physiology · 2024Review
- Common Pathophysiological Mechanisms and Treatment of Diabetic Gastroparesis.Journal of neurogastroenterology and motility · 2024Review
- Role of mechanoregulation in mast cell-mediated immune inflammation of the smooth muscle in the pathophysiology of esophageal motility disorders.American journal of physiology. Gastrointestinal and liver physiology · 2024Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND &
aimsMuscularis propria macrophages lie close to cells that regulate gastrointestinal motor function, including interstitial cells of Cajal (ICC) and myenteric neurons. In animal models of diabetic gastroparesis, development of delayed gastric emptying has been associated with loss of macrophages that express cytoprotective markers and reduced networks of ICC. Mice with long-term diabetes and normal gastric emptying have macrophages that express anti-inflammatory markers and have normal gastric ICC. Mice homozygous for the osteopetrosis spontaneous mutation in the colony-stimulating factor 1 gene (Csf1op/op) do not have macrophages; when they are given streptozotocin to induce diabetes, they do not develop delayed gastric emptying. We investigated whether population of the gastric muscularis propria of diabetic Csf1op/op mice with macrophages is necessary to change gastric emptying, ICC, and myenteric neurons and investigated the macrophage-derived factors that determine whether diabetic mice do or do not develop delayed gastric emptying.
methodsWild-type and Csf1op/op mice were given streptozotocin to induce diabetes. Some Csf1op/op mice were given daily intraperitoneal injections of CSF1 for 7 weeks; gastric tissues were collected and cellular distributions were analyzed by immunohistochemistry. CD45
resultsGastric muscularis propria from Csf1op/op mice given CSF1 contained macrophages; 11 of 15 diabetic mice given CSF1 developed delayed gastric emptying and had damaged ICC. In non-diabetic Csf1op/op mice, administration of CSF1 reduced numbers of gastric myenteric neurons but did not affect the proportion of nitrergic neurons or ICC. In diabetic Csf1op/op mice given CSF1 that developed delayed gastric emptying, the proportion of nitrergic neurons was the same as in non-diabetic wild-type controls. Medium conditioned by macrophages previously exposed to oxidative injury caused damage to ICC in cultured gastric muscularis propria from Csf1op/op mice; neutralizing antibodies against IL6R or TNF prevented this damage to ICC. CD45
conclusionsIn studies of Csf1op/op and wild-type mice with diabetes, we found delayed gastric emptying to be associated with increased production of inflammatory factors, and reduced production of anti-inflammatory factors, by macrophages, leading to loss of ICC.
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Registered trials
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