Contact dermatitis is the second most reported
occupational injury associated with workers compensation. Inflammatory
cytokines are closely involved with the development of
dermatitis, and their modulation could exacerbate skin damage, thus contributing to increased irritancy.
IL-6 is a pro-inflammatory
cytokine paradoxically associated with both skin healing and
inflammation. To determine what role this pleiotropic
cytokine plays in chemically-induced
irritant dermatitis,
IL-6 deficient (KO),
IL-6 over-expressing transgenic (TgIL6), and corresponding wild-type (WT) mice were exposed to
acetone or the irritants
JP-8 jet fuel or
benzalkonium chloride (BKC) daily for 7 days. Histological analysis of exposed skin was performed, as was tissue
mRNA and
protein expression patterns of inflammatory
cytokines via QPCR and multiplex ELISA. The results indicated that, following JP-8 exposure, IL-6KO mice had greatly increased skin IL-1β, TNFα, CCL2, CCL3, and CXCL1
mRNA and corresponding product
protein expression when compared to that of samples from WT counterparts and
acetone-exposed control mice. BKC treatment induced the expression of all
cytokines examined as compared to
acetone, with CCL2 significantly higher in skin from IL-6KO mice. Histological analysis showed that IL-6KO mice displayed significantly more inflammatory cell infiltration as compared to WT and TgIL6 mice in response to jet fuel. Analysis of
mRNA for the M2 macrophage marker CD206 indicated a 4-fold decrease in skin of IL-6KO mice treated with either
irritant as compared to WT. Taken together, these observations suggest that
IL-6 acts in an anti-inflammatory manner during
irritant dermatitis, and these effects are dependent on the chemical nature of the
irritant.