Scratch wound-induced CXCL8 upregulation is EGFR-dependent in keratinocytes

Wound healing is a sophisticated defense mechanism involving cell activation, migration, and proliferation, which are orchestrated by the coordinated production of various cytokines/chemokines such as chemokine (C-X-C motif) ligand 8 (CXCL8) [1] and chemokine (C-C motif) ligand 20 (CCL20) [2]. CXCL8 and CCL20 are potent chemoattractants for neutrophils and IL-17A –producing immune cells, respectively [1,3]. Notably, CXCL8, CCL20, and IL-17A accelerate epithelial wound healing [1,2,4]. In addition, neutrophils are the first immune cells to infiltrate wounded sites, and appropriate neutrophilic recruitment is critical for efficient wound healing [5,6].

Source: Journal of Dermatological Science - July 12, 2020 Category: Dermatology Authors: Kazuhisa Furue, Takamichi Ito, Gaku Tsuji, Takeshi Nakahara, Masutaka Furue Tags: Letter to the Editor Source Type: research