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
Department of Microbiology, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo 05508-900, Brazil.
Multidisciplinary Institute of Health, Federal University of Bahia, Vitória da Conquista 45029-094, Brazil.
Microorganisms. 2022 Oct 1;10(10):1962. doi: 10.3390/microorganisms10101962.
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 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 . 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-γ, interleukin (IL) 1β, IL-18, IL-6, and tumour necrosis factor alpha increased. The infection of PHKs by 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.
可从人类泌尿生殖道中分离出来。然而，其与宿主的相互作用仍知之甚少。在本研究中，我们旨在评估[具体感染物]感染对原代人角质形成细胞（PHK）的影响。对细胞周期不同阶段的细胞进行定量。评估参与细胞周期调控和细胞凋亡进程的蛋白质。评估编码与DNA损伤反应和Toll样受体途径相关蛋白质的基因表达，并对参与炎症反应的细胞因子进行定量。[具体感染物]感染后，在亚G0/G1期观察到更多的角质形成细胞。在存活的角质形成细胞中，感染导致G2/M期停滞；GADD45A表达增加，参与细胞凋亡调控和氧化应激的p53、p27和p21等蛋白质的表达也增加。在感染的原代人角质形成细胞中，与Toll样受体途径相关的基因表达发生变化，干扰素-γ、白细胞介素（IL）-1β、IL-18、IL-6和肿瘤坏死因子α的产生增加。[具体感染物]感染原代人角质形成细胞会导致细胞损伤，通过激活细胞损伤、氧化应激和Toll样受体的反应途径来影响细胞周期。总体而言，这种反应最终导致体外细胞增殖/活力降低。
