Epidermal Keratinocytes Regulate Bacterial Immune Responses and Host Defense Through EGFR
September 2017
in “
The journal of investigative dermatology/Journal of investigative dermatology
”
Studysummary This study using a genetic mouse model found that S. aureus-driven dysbiosis sustains inflammatory skin side effects from EGFR inhibitors, suggesting prophylactic antibiotic treatment may reduce rash severity without fixing barrier defects. Our plain-language summary of this paper — not a Tressless recommendation.
The study investigated the adverse effects of epidermal growth factor receptor inhibitors (EGFR-I) used in cancer therapy, particularly focusing on skin inflammation and hair loss. Using a genetic EGFR knock-out mouse model, researchers found that the collapse of the epidermal barrier and anti-microbial defense led to severe skin inflammation, exacerbated by a pathogenic dysbiosis primarily involving S. aureus. While antibiotic treatment improved the inflammatory phenotype, it did not address the barrier defects. The study suggested that prophylactic antibiotics could reduce rash severity in patients but emphasized the need to target EGFR-dependent mechanisms for better management of side effects and improved cancer treatment outcomes.
