Alcohol May Hinder Immune Response in Wound Healing
Mechanism may contribute to delayed wound closure, increased infection in drunk patients
MONDAY, April 14, 2014 (HealthDay News) -- Binge alcohol exposure impairs key components of the immune system involved in wound repair, which may account for the delayed wound healing seen in people who are injured while intoxicated, according to an animal study published online April 1 in Alcoholism: Clinical & Experimental Research.
Brenda J. Curtis, Ph.D., from Loyola University in Chicago, and colleagues gave C57BL/6 mice either intraperitoneal ethanol (EtOH; 2.2 g/kg) or saline using an episodic binge EtOH exposure protocol (three days EtOH, four days off, three days EtOH) to create a blood alcohol concentration (BAC) of 300 mg/dL at the time of wounding. Six 3-mm full-thickness dorsal wounds were created and immediately treated topically with 10 µL of sterile saline (control) or diluted Staphylococcus aureus (1 × 104 CFU/wound). Twenty-four hours post-injury, wounds were harvested to evaluate wound area, neutrophil and macrophage accumulation, cytokine protein levels, cathelicidin-related antimicrobial peptide (CRAMP) and kallikrein epidermal proteases (KLK5 and KLK7).
The researchers found that EtOH-treated mice showed delayed wound closure, decreased macrophage accumulation, and impaired production of macrophage inflammatory protein-1α, compared to control mice. Skin from EtOH-treated mice also had a reduction in the abundance of epidermal CRAMP and KLK7.
"These findings suggest that EtOH exposure hinders several distinct components of the innate immune response, including phagocyte recruitment and chemokine/cytokine and AMP production," the authors write.