Fibroblasts resist Staphylococcus aureus on the skin surface by responding to interleukin-1 and recruiting neutrophils

This apparent paradox suggests a strong host defense system which prevents SA from invading the dermis. In this study, we investigate how the skin detects and responds to superficial SA exposure.

Using unbiased transcriptomic, biochemical, and phosphoproteomic analyses, followed by validation of the identified activation pathways in human and mouse models, we discovered that fibroblast recognition of interleukin-1 is essential for skin inflammation in response to topical SA. Deletion or blockade of the interleukin-1 receptor in fibroblasts in vitro abolished the change in gene expression and reduced chemokine production.