Chronic psychological stress aggravates psoriasis-like skin inflammation via overactivation of ß<sub>2</sub>-adrenoceptor and nuclear factor kappa B pathways.

Donato-Trancoso, Aline; Cristina de Souza Ribeiro, Bianca; Barrozo do Canto, Fábio; de Souza Nogueira, Jeane; Romana-Souza, Bruna

Chronic psychological stress aggravates psoriasis-like skin inflammation via overactivation of ß₂-adrenoceptor and nuclear factor kappa B pathways.

Donato-Trancoso, Aline; Cristina de Souza Ribeiro, Bianca; Barrozo do Canto, Fábio; de Souza Nogueira, Jeane; Romana-Souza, Bruna.

Afiliação

Donato-Trancoso A; Department of Histology and Embryology, Rio de Janeiro State University, Rio de Janeiro, Brazil.
Cristina de Souza Ribeiro B; Department of Histology and Embryology, Rio de Janeiro State University, Rio de Janeiro, Brazil.
Barrozo do Canto F; Department of Immunobiology, Federal Fluminense University, Niterói, Brazil.
de Souza Nogueira J; Histocompatibility and Cryopreservation Laboratory, Rio de Janeiro State University, Rio de Janeiro, Brazil.
Romana-Souza B; Department of Histology and Embryology, Rio de Janeiro State University, Rio de Janeiro, Brazil.

Scand J Immunol ; 97(4): e13258, 2023 Apr.

Article em En | MEDLINE | ID: mdl-39007953

ABSTRACT

ABSTRACT

The relationship between psoriasis severity and psychological stress has been described in several studies. However, the mechanism by which chronic stress exacerbates psoriasis is not completely understood. This study aimed at investigating whether chronic psychological stress can aggravate psoriasis-like skin inflammation. Mice were subjected to a restraint stress model and topically treated with imiquimod (IMQ). Differentiated human keratinocytes were treated with high epinephrine levels and IMQ in vitro. Stress aggravated macroscopic features and the increase in epidermal thickness induced by IMQ in mouse skin. The increase in NF-κB and IL-17A expression induced by IMQ was potentiated by chronic stress in mouse skin. The skin of stressed mice treated with IMQ showed higher levels of ß2-adrenergic receptors (ß2-AR). In human keratinocytes, high epinephrine levels exacerbated the increase in the levels of ß2-AR and IL-17A induced by IMQ. ß-AR antagonist reversed the effects of chronic stress in IMQ-induced inflammation both in vivo and in vitro. In conclusion, stress-stimulated overactivation of the ß2-AR and NF-κB pathways potentiates a Th1/Th17 profile leading to an exacerbation of psoriasis.

Assuntos

Imiquimode; Interleucina-17; Queratinócitos; NF-kappa B; Psoríase; Receptores Adrenérgicos beta 2; Transdução de Sinais; Estresse Psicológico; Animais; Humanos; Masculino; Camundongos; Modelos Animais de Doenças; Epinefrina; Inflamação/imunologia; Inflamação/metabolismo; Interleucina-17/metabolismo; Queratinócitos/metabolismo; Queratinócitos/imunologia; NF-kappa B/metabolismo; Psoríase/imunologia; Psoríase/metabolismo; Receptores Adrenérgicos beta 2/metabolismo; Pele/patologia; Pele/imunologia; Pele/metabolismo; Estresse Psicológico/complicações; Estresse Psicológico/imunologia; Células Th1/imunologia; Células Th17/imunologia

Palavras-chave

cyclic adenosine monophosphate; interleukin17A; psoriasis; psychological stress; ßAdrenergic receptor

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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Psoríase / Estresse Psicológico / Transdução de Sinais / Queratinócitos / NF-kappa B / Receptores Adrenérgicos beta 2 / Interleucina-17 / Imiquimode Limite: Animals / Humans / Male Idioma: En Revista: Scand J Immunol Ano de publicação: 2023 Tipo de documento: Article País de afiliação: Brasil País de publicação: Reino Unido

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