Mycoplasma hominis Causes DNA Damage and Cell Death in Primary Human Keratinocytes

Autor(es)

Amorim, Aline Teixeira ; Lino, Vanesca de Souza ; Marques, Lucas Miranda ; Martins, Davi Jardim ; Braga Junior, Antonio Carlos Ricardo ; Campos, Guilherme Barreto ; Oliveira, Caline Novais Teixeira ; Boccardo, Enrique ; Timenetsky, Jorge

• Tipo de documento: Artigo Científico
• Fonte: MICROORGANISMS; v. 10, n. 10, p. 16-pg., 2022-10-01.

Resumo

Mycoplasma hominis can be isolated from the human urogenital tract. However, its interaction with the host remains poorly understood. In this study, we aimed to assess the effects of M. hominis infection on primary human keratinocytes (PHKs). Cells were quantified at different phases of the cell cycle. Proteins involved in cell cycle regulation and apoptosis progression were evaluated. The expression of genes encoding proteins that are associated with the DNA damage response and Toll-like receptor pathways was evaluated, and the cytokines involved in inflammatory responses were quantified. A greater number of keratinocytes were observed in the Sub-G0/G1 phase after infection with M. hominis. In the viable keratinocytes, infection resulted in G2/M-phase arrest; GADD45A expression was increased, as was the expression of proteins such as p53, p27, and p21 and others involved in apoptosis regulation and oxidative stress. In infected PHKs, the expression of genes associated with the Toll-like receptor pathways showed a change, and the production of IFN-gamma, interleukin (IL) 1 beta, IL-18, IL-6, and tumour necrosis factor alpha increased. The infection of PHKs by M. hominis causes cellular damage that can affect the cell cycle by activating the response pathways to cellular damage, oxidative stress, and Toll-like receptors. Overall, this response culminated in the reduction of cell proliferation/viability in vitro. (AU)

• Processo FAPESP: 14/05071-6 - Avaliação da participação dos Mollicutes e outros microrganismos de interesse genital na endometriose humana
• Beneficiário: Jorge Timenetsky
• Modalidade de apoio: Auxílio à Pesquisa - Regular