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Atopic dermatitis-like epicutaneous infection with S. aureus in WT and eosinophil KO mice

ABSTRACT: Investigation of the pathways involved in eosinophil-mediated inflammation in S. aureus epicutaneous infection

ORGANISM(S): Mus musculus

PROVIDER: GSE216246 | GEO | 2024/01/29

REPOSITORIES: GEO

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Atopic dermatitis-like epicutaneous infection with S. aureus in WT and eosinophil KO mice

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Project description:Background: Atopic dermatitis (AD) is a common inflammatory skin disease with a TH2 immune polarity and is often colonized with Staphylococcus aureus. Despite recent advances in understanding Staphylococcus species infection and the impact of polar TH cytokines on the skin, the interactions between these factors in AD pathology are poorly understood. Methods: AD-related key immune biomarkers were measured by quantitative real-time PCR in human keratinocytes exposed heat-killed S. epidermidis or S. aureus with/without polar T-cell derived cytokines such as IFN-γ (TH1), IL-4/IL-13 (TH2), and IL-22 (TH22). Further analysis was performed by RNA-sequencing to define broader responses in both Staphylococcus species and polar cytokines. The similarity of gene expression patterns in AD skin lesions and stimulated keratinocytes was evaluated by gene-set variation analysis (GSVA). Results: Gene expression analysis exhibited distinct immune responses in keratinocytes depending on individual bacterial or polar cytokine exposure. Besides, numerous genes were synergistically upregulated by the combination exposure of bacteria and polar TH cytokines. Moreover, GSVA revealed that combined exposure of S. aureus and IL-4 + IL-13 exhibited significantly higher correlations with a genomic signature of AD skin lesions than their single exposure or combinations of other polar TH cytokines. Conclusions: Our findings provide novel insights into AD-related transcriptional activation and illustrate a potentially novel pathogenic function of S. aureus and IL-4/IL-13 interactions in AD.

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Project description:Microbial exposure at barrier interfaces drives development and balance of the immune system but the consequences of local infections for systemic immunity and secondary inflammation are unclear. Here, we show that epicutaneous exposure to the bacterium Staphylococcus aureus persistently shapes the immune system of mice with specific impact on progenitor and mature bone marrow neutrophil and eosinophil populations. The infection-imposed changes in eosinophils were long-lasting and associated with functional as well as imprinted epigenetic and metabolic changes. Bacterial exposure enhanced skin allergic sensitization and resulted in exacerbated allergen-induced lung inflammation. S. aureus-mediated functional bone marrow eosinophil reprogramming and pulmonary allergen responses were driven by the alarmin interleukin 33 and the complement cleavage fragment C5a. Our study highlights the systemic impact of skin inflammation and reveals eosinophil progenitor training and organ-crosstalk mechanisms that modulate systemic responses to allergens.

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Repeated monthly epicutaneous challenges with diphenylcyclopropenone (DPCP).

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Repeated monthly epicutaneous challenges with diphenylcyclopropenone (DPCP).

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