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Nutritional Immunology

Dietary Zinc Alters Early Inflammatory Responses during Cutaneous Wound Healing in Weanling CD-1 Mice^1,2

Yunsook Lim^*,, Mark Levy^*, and Tammy M. Bray^*,,3

^* Department of Human Nutrition, The Ohio State University, Columbus, OH and Linus Pauling Institute, Oregon State University, Corvallis, OR

³To whom correspondence and reprint requests should be addressed. E-mail: tammy.bray{at}oregonstate.edu.

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)B activation, reduced expression of proinflammatory cytokines [interleukin (IL)-1ß and tumor necrosis factor (TNF)-], 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)B, IL-1ß, and TNF- and infiltration of neutrophils at the wound site of mice fed a diet containing <1 (deficient), 50 (control), 500, or 1000 µg zinc/g diet. Zinc deficiency reduced the rate of wound closure and mRNA levels of IL-1ß and TNF- and attenuated infiltration of neutrophils at the wound site compared with controls. Interestingly, zinc supplementation at 1000 µg/g delayed the rate of wound closure and decreased mRNA levels of TNF- and infiltration of neutrophils compared with mice fed the control diet. These findings demonstrate that zinc deficiency and high-dose zinc supplementation delay wound healing as a result of altered inflammatory responses and suggest that adequate zinc supplementation may have beneficial effects on the inflammatory responses to enhance cutaneous wound healing.

KEY WORDS: • wound healing • zinc • inflammation • proinflammatory cytokines