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Interleukin-17 governs hypoxic adaptation of injured epithelium [bulk RNA-seq]

ABSTRACT: RORgt deficency impaired wound re-epithelialization. We adopted low-input RNA-seq of purified wound epithelium to explore the underlying epithelial cell functional difference between wild type and RORgt deficient mice during wound healing.

ORGANISM(S): Mus musculus

PROVIDER: GSE166946 | GEO | 2021/02/18

REPOSITORIES: GEO

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Interleukin-17 governs hypoxic adaptation of injured epithelium.

Project description:Mammalian cells autonomously activate hypoxia-inducible transcription factors (HIFs) to ensure survival in low-oxygen environments. We report here that injury-induced hypoxia is insufficient to trigger HIF1α in damaged epithelium. Instead, multimodal single-cell and spatial transcriptomics analyses and functional studies reveal that retinoic acid-related orphan receptor γt+ (RORγt+) γδ T cell-derived interleukin-17A (IL-17A) is necessary and sufficient to activate HIF1α. Protein kinase B (AKT) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling proximal of IL-17 receptor C (IL-17RC) activates mammalian target of rapamycin (mTOR) and consequently HIF1α. The IL-17A-HIF1α axis drives glycolysis in wound front epithelia. Epithelial-specific loss of IL-17RC, HIF1α, or blockade of glycolysis derails repair. Our findings underscore the coupling of inflammatory, metabolic, and migratory programs to expedite epithelial healing and illuminate the immune cell-derived inputs in cellular adaptation to hypoxic stress during repair.

| S-EPMC9753231 | biostudies-literature

Interleukin-17 governs hypoxic adaptation of injured epithelium

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-18 | GSE166950 | GEO

Interleukin-17 governs hypoxic adaptation of injured epithelium [spatial transcriptomics]

Project description:To define the gene signature and spatial architecture of the skin after injury, we performed spatial transcriptomics from mouse unwounded and wounded skin.

2021-02-18 | GSE166948 | GEO

Interleukin-17 governs hypoxic adaptation of injured epithelium

Project description:Interleukin-17 governs hypoxic adaptation of injured epithelium

| PRJNA702447 | ENA

Interleukin-17 governs hypoxic adaptation of injured epithelium [CITE-seq & single-cell RNA-seq]

Project description:To define the composition of “first responder” lymphocytes that may engage in crosstalk with injured epithelium we profiled the lymphoytes from unwounded health skin and skin from different time points after wounding with CITE-seq and single-cell RNA-sequencing.

2021-02-18 | GSE166949 | GEO

Interleukin-17 governs hypoxic adaptation of injured epithelium [spatial transcriptomics]

Project description:Interleukin-17 governs hypoxic adaptation of injured epithelium [spatial transcriptomics]

| PRJNA702458 | ENA

Interleukin-17 governs hypoxic adaptation of injured epithelium [bulk RNA-seq]

Project description:Interleukin-17 governs hypoxic adaptation of injured epithelium [bulk RNA-seq]

| PRJNA702456 | ENA

Interleukin-17 governs hypoxic adaptation of injured epithelium [CITE-seq & single-cell RNA-seq]

Project description:Interleukin-17 governs hypoxic adaptation of injured epithelium [CITE-seq & single-cell RNA-seq]

| PRJNA702457 | ENA

Interleukin-17 limits hypoxia-inducible factor 1? and development of hypoxic granulomas during tuberculosis.

Project description:Mycobacterium tuberculosis (Mtb) is a global health threat, compounded by the emergence of drug-resistant strains. A hallmark of pulmonary tuberculosis (TB) is the formation of hypoxic necrotic granulomas, which upon disintegration, release infectious Mtb. Furthermore, hypoxic necrotic granulomas are associated with increased disease severity and provide a niche for drug-resistant Mtb. However, the host immune responses that promote the development of hypoxic TB granulomas are not well described. Using a necrotic Mtb mouse model, we show that loss of Mtb virulence factors, such as phenolic glycolipids, decreases the production of the proinflammatory cytokine IL-17 (also referred to as IL-17A). IL-17 production negatively regulates the development of hypoxic TB granulomas by limiting the expression of the transcription factor hypoxia-inducible factor 1? (HIF1?). In human TB patients, HIF1? mRNA expression is increased. Through genotyping and association analyses in human samples, we identified a link between the single nucleotide polymorphism rs2275913 in the IL-17 promoter (-197G/G), which is associated with decreased IL-17 production upon stimulation with Mtb cell wall. Together, our data highlight a potentially novel role for IL-17 in limiting the development of hypoxic necrotic granulomas and reducing disease severity in TB.

| S-EPMC5841875 | biostudies-literature

Setd2 Epidermal Deficiency Promotes Cutaneous Wound Healing via Activation of AKT/mTOR Signaling (ChIP-Seq)

Project description:Skin wound healing is one of the major prevalent medical problems in the worldwide. Wound healing involves multi-process synergy and re-epithelialization is an essential part of wound healing. Histone H3K36 tri-methylase Setd2 has been extensively studied in different biological processes and diseases. However, the function of Setd2 in the wound healing remains unclear. To elucidate the biological role of Setd2 in the skin wound healing, conditional gene targeting was employed to establish epidermis-specific Setd2-deficient mice. We found that Setd2 deficiency resulted in accelerated re-epithelialization during cutaneous wound healing by promoting keratinocytes proliferation and migration. Furthermore, we demonstrated that loss of Setd2 activated the AKT/mTOR pathway, and pharmacological inhibitions of AKT and mTOR with MK2206 and rapamycin delayed wound closure, respectively. In conclusion, our results reveal the essential role of Setd2 in skin wound healing that is Setd2 loss promotes cutaneous wound healing via activation of AKT/mTOR signaling.

2020-12-25 | GSE163858 | GEO

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