ArticlePLoS pathogens2023
Choline metabolism underpins macrophage IL-4 polarization and RELMα up-regulation in helminth infection.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Helminth infection induces RELMα-dependent adipose tissue transcriptional reprogramming and protection against diet-induced obesity.bioRxiv : the preprint server for biology · 2026Article
- Dysregulated immunometabolism in gut inflammation.Acta biochimica et biophysica Sinica · 2026Review
- Maternal choline supplementation in neurodevelopmental disorders: mechanistic insights from animal models and future directions.Nutritional neuroscience · 2025Review
- Choline metabolism disorder induced by Prevotella is a risk factor for endometrial cancer in women with polycystic ovary syndrome.Molecular biology reports · 2025Observational
- Choline in immunity: a key regulator of immune cell activation and function.Frontiers in immunology · 2025Review
- Eating for immunity: how diet shapes our defenses.Current opinion in immunology · 2024Review
- Maternal choline supplementation modulates cognition and induces anti-inflammatory signaling in the prefrontal cortices of adolescent rats exposed to maternal immune activation.Brain, behavior, & immunity - health · 2024Article
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Authors and funding
22 authors at 2 institutions in 2 countries.
Funding
Abstract
Type 2 cytokines like IL-4 are hallmarks of helminth infection and activate macrophages to limit immunopathology and mediate helminth clearance. In addition to cytokines, nutrients and metabolites critically influence macrophage polarization. Choline is an essential nutrient known to support normal macrophage responses to lipopolysaccharide; however, its function in macrophages polarized by type 2 cytokines is unknown. Using murine IL-4-polarized macrophages, targeted lipidomics revealed significantly elevated levels of phosphatidylcholine, with select changes to other choline-containing lipid species. These changes were supported by the coordinated up-regulation of choline transport compared to naïve macrophages. Pharmacological inhibition of choline metabolism significantly suppressed several mitochondrial transcripts and dramatically inhibited select IL-4-responsive transcripts, most notably, Retnla. We further confirmed that blocking choline metabolism diminished IL-4-induced RELMα (encoded by Retnla) protein content and secretion and caused a dramatic reprogramming toward glycolytic metabolism. To better understand the physiological implications of these observations, naïve or mice infected with the intestinal helminth Heligmosomoides polygyrus were treated with the choline kinase α inhibitor, RSM-932A, to limit choline metabolism in vivo. Pharmacological inhibition of choline metabolism lowered RELMα expression across cell-types and tissues and led to the disappearance of peritoneal macrophages and B-1 lymphocytes and an influx of infiltrating monocytes. The impaired macrophage activation was associated with some loss in optimal immunity to H. polygyrus, with increased egg burden. Together, these data demonstrate that choline metabolism is required for macrophage RELMα induction, metabolic programming, and peritoneal immune homeostasis, which could have important implications in the context of other models of infection or cancer immunity.
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