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Glutamine metabolism suppresses neutrophil recruitment via epigenetic regulation to control inflammatory resolution and skin repair [D1D3 RNAseq]

ABSTRACT: Tissue repair requires the resolution of inflammation. However, the molecular mechanisms that attenuate inflammation in vivo are not fully understood. Here, we identify that glutamine metabolism suppresses neutrophil recruitment to abrogate inflammation and drive tissue repair. Integrated metabolomic and transcriptional profiling identified glutamine metabolism as a key feature of macrophages during inflammatory resolution. Dietary depletion studies and conditional deletion of glutaminase (Gls), the essential enzyme involved in glutamine metabolism, in innate immune cells in mice reveals an essential role for glutamine metabolism in suppressing inflammation and promoting tissue repair. Genes involved in neutrophil recruitment are upregulated in macrophages lacking Gls and in foot ulcers of diabetic patients. Multimodal single cell transcriptomics and epigenomics reveals that Gls is required for chromatin remodeling of neutrophil recruitment genes in innate immune cells during resolution of inflammation. These findings highlight the role of glutamine metabolism in controlling cellular communication during tissue repair and suppressing neutrophil recruitment to advance inflammation resolution.

ORGANISM(S): Mus musculus

PROVIDER: GSE289200 | GEO | 2026/02/01

REPOSITORIES: GEO

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Project description:Dunster2014 - WBC Interactions (Model1) This is a sub-model of a three-step inflammatory response modelling study. The model includes distinct populations of white blood cells namely, macrophages and active and apoptotic neutrophil populations. Neutrophil apoptosis rate is predicted to be crucial for the qualitative nature of the system. This model is described in the article: The resolution of inflammation: a mathematical model of neutrophil and macrophage interactions. Dunster JL, Byrne HM, King JR. Bull. Math. Biol. 2014 Aug; 76(8): 1953-1980 Abstract: There is growing interest in inflammation due to its involvement in many diverse medical conditions, including Alzheimer's disease, cancer, arthritis and asthma. The traditional view that resolution of inflammation is a passive process is now being superceded by an alternative hypothesis whereby its resolution is an active, anti-inflammatory process that can be manipulated therapeutically. This shift in mindset has stimulated a resurgence of interest in the biological mechanisms by which inflammation resolves. The anti-inflammatory processes central to the resolution of inflammation revolve around macrophages and are closely related to pro-inflammatory processes mediated by neutrophils and their ability to damage healthy tissue. We develop a spatially averaged model of inflammation centring on its resolution, accounting for populations of neutrophils and macrophages and incorporating both pro- and anti-inflammatory processes. Our ordinary differential equation model exhibits two outcomes that we relate to healthy and unhealthy states. We use bifurcation analysis to investigate how variation in the system parameters affects its outcome. We find that therapeutic manipulation of the rate of macrophage phagocytosis can aid in resolving inflammation but success is critically dependent on the rate of neutrophil apoptosis. Indeed our model predicts that an effective treatment protocol would take a dual approach, targeting macrophage phagocytosis alongside neutrophil apoptosis. This model is hosted on BioModels Database and identified by: BIOMD0000000616. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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Glutamine metabolism suppresses neutrophil recruitment via epigenetic regulation to control inflammatory resolution and skin repair [D1D3 RNAseq]

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