Dietary zinc alters early inflammatory responses during cutaneous wound healing in weanling CD-1 mice

Zinc deficiency is a well-known health problem associated with delayed wound healing, yet the precise mechanisms that underlie the delay remain unknown. We hypothesized that zinc deficiency delays wound healing as a result of decreased nuclear factor (NF)[kappa]B activation, reduced expression of proinflammatory cytokines [interleukin (IL)-1[beta] and tumor necrosis factor (TNF)-[alpha]], and a decrease in neutrophil infiltration during the early stage of cutaneous wound healing. We used a cutaneous, full-thickness excisional wound model in CD-1 mice to examine the rate of wound closure as well as mRNA levels of inhibitory (I)[kappa]B[alpha], IL-1[beta], and TNF-[alpha] and infiltration of neutrophils at the wound site of mice fed a diet containing KEY WORDS: * wound healing * zinc * inflammation * proinflammatory cytokines