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Influence of substance-P on cultured sebocytes

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Abstract

Acne is a complex, chronic and common skin disorder of pilosebaceous units. Although it is known that exacerbation of acne results from emotional stress, the nature of the association between stress and acne remains unclear. This is due in part to the lack of substantial evidence regarding the participation of cutaneous neurogenic factors in the pathogenesis of acne. Culture of sebocytes provides a new insight into the participation of neuropeptides, notably substance P (SP), in the pathophysiology of acne. To examine the possible involvement of neurogenic factors in the pathogenesis of acne, we used immunohistochemistry and RT-PCR to compare the expression of interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), peroxisome proliferators activated receptors-γ (PPAR-γ) on the cultured sebocytes stimulated by SP. IL-1 is primarily proinflammatory cytokines to stimulate the expression of genes associated with inflammation. IL-6 is a pleiotropic cytokine with a wide range of biological activities and regulates inflammation. TNF-α is a pleiotropic pro-inflammatory cytokine that exerts multiple biologic effects. PPAR-γ is a nuclear hormone receptor and plays a unique role in stimulating sebocyte lipogenesis. More numerous immunoreactivity to IL-1, IL-6, TNF-α and PPAR-γ and increased RNA amplification for IL-1, IL-6, TNF-α and PPAR-γ were observed after addition of SP compared with the control. This study reveals that SP is involved in the pathogenesis of acne.

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Authors and Affiliations

  1. Department of Dermatology, Kyungpook National University School of Medicine, 700-721 Sam-duck 2 Ga 50, Jung-gu, Daegu, Republic of Korea

    Weon Ju Lee, Hong Dae Jung, Hyun Joo Lee, Byung Soo Kim, Seok-Jong Lee & Do Won Kim

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  1. Weon Ju Lee
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  2. Hong Dae Jung
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  3. Hyun Joo Lee
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  4. Byung Soo Kim
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  5. Seok-Jong Lee
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  6. Do Won Kim
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Correspondence to Weon Ju Lee.

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Lee, W.J., Jung, H.D., Lee, H.J. et al. Influence of substance-P on cultured sebocytes. Arch Dermatol Res 300, 311–316 (2008). https://doi.org/10.1007/s00403-008-0854-1

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  • DOI: https://doi.org/10.1007/s00403-008-0854-1

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