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Epithelial-Immune Metabolic Codependency Fuels Inflammatory Disease [Spatial Transcriptomics]

ABSTRACT: Epithelial-Immune Metabolic Codependency Fuels Inflammatory Disease [Spatial Transcriptomics]

PROVIDER: PRJNA996584 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25342012.fastq.gz	Fastqsanger.gz
	SRR25342013.fastq.gz	Fastqsanger.gz
	SRR25342014.fastq.gz	Fastqsanger.gz
	SRR25342015.fastq.gz	Fastqsanger.gz

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Epithelial-Immune Metabolic Codependency Fuels Inflammatory Disease [Spatial Transcriptomics]

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Dickkopf1 fuels inflammatory cytokine responses

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Epithelial-Immune Metabolic Codependency Fuels Inflammatory Disease [Bulk RNA-seq]

Project description:Inflammatory skin diseases are spurred by unchecked immune-epithelial circuits. Although the function of cytokine and chemokine signals in facilitating this crosstalk is well established, the specific metabolic mediators involved and their simultaneous contribution to dysregulation of these two distinct cellular compartments is unclear. Here, we employed scRNA-seq, spatial transcriptomics, and immunofluorescence across multiple disease indications to elucidate a dysfunctional epithelial state marked by Hypoxia Inducible Factor 1 alpha (HIF1⍺). Ex vivo HIF1⍺ blockade of human Psoriasis (PsO) lesions led to a reduction in pathological gene expression via modulation of glucose metabolism. Epidermal-specific loss of HIF1⍺ or its transcriptional target, glucose transporter 1, curtailed both epidermal pathology and the cutaneous immune response in murine PsO. Glycolytic metabolism sustained epithelial hyperproliferation and differentiation, while lactate, its terminal product, was crucial for sustaining Type 17 response. Notably, inhibition of lactate dehydrogenase A or the lactate transporters MCT1/4 selectively attenuated the Type 17 response, underscoring a divergent requirement for glucose and lactate in epithelial and immune cells, respectively. Collectively, these findings identify therapeutically targetable immune-epithelial circuits by unveiling a remarkable coordination of metabolic processed between the epithelial and immune compartments in inflammatory skin disease.

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Project description:Many human diseases, including cancer, share an inflammatory component but the molecular underpinnings remain incompletely understood. We report that physiological and pathological Dickkopf1 (DKK1) activity fuels inflammatory cytokine responses in cell models, mice and humans. DKK1 maintains the elevated inflammatory tone of cancer cells and is required for mounting cytokine responses following ligation of toll-like and cytokine receptors. DKK1-controlled inflammation derives from cell-autonomous mechanisms, which involve SOCS3-restricted, nuclear RelA (p65) activity. We translate these findings to humans by showing that genetic DKK1 variants are linked to elevated cytokine production across healthy populations. Finally, we find that genetic deletion of DKK1 but not pharmacological neutralization of soluble DKK1 ameliorates inflammation and disease trajectories in a mouse model of endotoxemia. Collectively, our study identifies a cell-autonomous function of DKK1 in the control of the inflammatory response, which is conserved between malignant and non-malignant cells and may be exploited therapeutically in the future.

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