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Transcriptional profiling of mouse skin upon antibody-mediated neutrophil depletion

ABSTRACT: Transcriptional profiling of mouse skin upon antibody-mediated neutrophil depletion

PROVIDER: PRJNA1134218 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29804961.fastq.gz	Fastqsanger.gz
	SRR29804962.fastq.gz	Fastqsanger.gz

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Transcriptional profiling of mouse skin upon antibody-mediated neutrophil depletion

Project description:Neutrophils patrol healthy tissues and confer local defense upon perturbations. Recent evidence suggests that they participate in tissue-specific structural programs in addition to their indispensable role in immunity.The goal of this study is to evaluate the effect of neutrophils in healthy mouse skin by comparing the transcriptional landscape of naive skin to neutrophil-depleted skin.

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Project description:Psoriasis is a chronic inflammatory skin disease affecting millions of people worldwide. Although growing evidence links chronic inflammation with increased cancer risk, the association between psoriasis and cutaneous squamous cell carcinoma (cSCC) is still elusive. Using cell transplantation and chemical-induced models of cSCC combined with inducible genetically engineered mouse models (GEMMs) of psoriasis, we investigated how chronic skin and systemic inflammation affects squamous skin tumor initiation and progression. Here we show that in the context of severe psoriasis-like disease, neutrophil-dependent inflammation prevents squamous skin tumor development. Cellular and molecular analyses of psoriasis-like skin at the tumor initiation stage revealed a marked infiltration of CD54–expressing neutrophils, associated with the release of cytotoxic granules and neutrophil extracellular traps (NETs), as well as enhanced senescence and the expression of senescence-associated secretory phenotype (SASP) in keratinocytes. Furthermore, single-cell RNA sequencing demonstrated that inflammatory N1-like neutrophils mediate re-programming of the cell-cell communication networks, while keratinocytes displayed diminished responsiveness to mitogenic signals, including EGF and WNT. Importantly, neutrophil depletion ameliorated psoriasis-like inflammation, abolished the senescence-like phenotype in keratinocytes and restored tumor growth. We propose that the release of neutrophil granules and NETs in psoriasis-like skin eliminate tumor cells and/or mediate oxidative and inflammatory stress-induced senescence in keratinocytes, thereby preventing tumor growth. Taken together, we have defined an innate control of skin tumorigenesis in psoriasis-like disease, which will be relevant for developing cancer prevention strategies.

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