BackgroundA single, effective therapeutic regimen for keloids has not been established yet, and the development of novel therapeutic approaches is expected. Butyrate, a short-chain fatty acid, and docosahexaenoic acid (DHA), a ω-3 polyunsaturated fatty acid, play multiple anti-inflammatory and anticancer roles via their respective mechanisms of action.ObjectiveIn this study, we evaluated the antifibrogenic effects of their single and combined use on keloid fibroblasts.MethodsKeloid fibroblasts were treated with butyrate (0-16 mM) and/or DHA (0-100 µM) for 48 or 96 h.ResultsButyrate inhibited cell proliferation, and α-smooth muscle actin (α-SMA) and type III collagen expressions, with inhibition of the transforming growth factor (TGF)-β1 and TGF-β type I receptor expressions and increased prostaglandin E2 with upregulation of cyclooxygenase-1 expression with induction of histone acetylation. DHA inhibited α-SMA, type III collagen, and TGF-β type I receptor expressions. Then, the butyrate/DHA combination augmented the antifibrogenic effects, resulting in additional inhibition of α-SMA, type I and III collagen expressions, with strong disruption of stress fiber and apoptosis induction. Moreover, the butyrate/DHA combination inhibited the cyclooxygenase-2 expression, suggesting stronger anti-inflammatory effect than each monotherapy.Study limitationsActivation in keloid tissue is affected not only by fibroblasts but also by epithelial cells and immune cells. Evaluation of the effects by butyrate and DHA in these cells or in an in vivo study is required.ConclusionThis study demonstrated that butyrate and docosahexaenoic acid have antifibrogenic effects on keloid fibroblasts and that these may exert therapeutic effects for keloid.

The patient was a 68-year-old woman who had experienced recurrent febrile episodes since 66 years of age. Despite various examinations and treatments, the etiology remained unclear. Further examinations following another referral failed to uncover the cause. Therefore, despite her age, it was presumed that she had familial Mediterranean fever. An analysis of the familial Mediterranean fever (MEFV) gene detected heterozygous L110P, E148Q, and R202Q mutations. No further febrile episodes occurred after colchicine treatment was initiated. Familial Mediterranean fever presenting in patients in their sixties is extremely rare.

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