Injury, dysbiosis, and filaggrin deficiency drive skin inflammation through keratinocyte IL-1α release.

ABSTRACT:

Background

Atopic dermatitis (AD) is associated with epidermal barrier defects, dysbiosis, and skin injury caused by scratching. In particular, the barrier-defective epidermis in patients with AD with loss-of-function filaggrin mutations has increased IL-1α and IL-1β levels, but the mechanisms by which IL-1α, IL-1β, or both are induced and whether they contribute to the aberrant skin inflammation in patients with AD is unknown.

Objective

We sought to determine the mechanisms through which skin injury, dysbiosis, and increased epidermal IL-1α and IL-1β levels contribute to development of skin inflammation in a mouse model of injury-induced skin inflammation in filaggrin-deficient mice without the matted mutation (ft/ft mice).

Methods

Skin injury of wild-type, ft/ft, an

SUBMITTER: Archer NK 

PROVIDER: S-EPMC6424655 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature