Mendes Ana Clara, Ciccone Marcone, Gazolla Bruna, Bahia Diana
Departamento de Genética, Ecologia e Evolução, Instituto de Ciencias Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Front Cell Dev Biol. 2020 Jun 9;8:439. doi: 10.3389/fcell.2020.00439. eCollection 2020.
The World Health Organization (WHO) has estimated that in 2016, there were 87 million new cases of gonorrhea. Gonorrhea is caused by the sexually transmitted human-exclusive agent , a Gram-negative diplococcus that causes cervicitis in females and urethritis in males and may lead to more severe complications. Currently, there is no vaccine against . Its resistance to antibiotics has been increasing in the past few years, reducing the range of treatment options. requires a surface protein/receptor (Opa proteins, porin, Type IV pili, LOS) to adhere to and invade epithelial cells. During invasion and transcytosis, is targeted by the autophagy pathway, a cellular maintenance process which balances sources of energy at critical times by degrading damaged organelles and macromolecules in the lysosome. Autophagy is an important host defense mechanism which targets invading pathogens. Based on transmission electron microscopy (TEM) analysis, the intracellular bacteria occupy the autophagosome, a double-membraned vesicle that is formed around molecules or microorganisms during macroautophagy and fuses with lysosomes for degradation. Most of the gonococci end up in autolysosomes for degradation, but a subpopulation of the intracellular bacteria inhibits the maturation of the autophagosome and its fusion with lysosomes by activating mTORC1 (a known suppressor of the autophagy signaling), thus escaping autophagic elimination. This mini review focuses on the cellular features of during epithelial cell invasion, with a particular focus on how evades the autophagy pathway.
世界卫生组织(WHO)估计,2016年有8700万例新的淋病病例。淋病由性传播的专性人类病原体引起,这是一种革兰氏阴性双球菌,可导致女性宫颈炎和男性尿道炎,并可能引发更严重的并发症。目前,尚无针对该病原体的疫苗。在过去几年中,它对抗生素的耐药性不断增加,减少了治疗选择的范围。该病原体需要一种表面蛋白/受体(Opa蛋白、孔蛋白、IV型菌毛、脂寡糖)来黏附并侵入上皮细胞。在入侵和跨细胞转运过程中,该病原体成为自噬途径的作用靶点,自噬是一种细胞维持过程,通过在溶酶体中降解受损细胞器和大分子,在关键时期平衡能量来源。自噬是一种针对入侵病原体的重要宿主防御机制。基于透射电子显微镜(TEM)分析,细胞内细菌占据自噬体,自噬体是一种双膜囊泡,在巨自噬过程中围绕分子或微生物形成,并与溶酶体融合以进行降解。大多数淋球菌最终进入自溶酶体进行降解,但细胞内细菌的一个亚群通过激活mTORC1(一种已知的自噬信号抑制因子)来抑制自噬体的成熟及其与溶酶体的融合,从而逃避自噬清除。这篇小型综述聚焦于该病原体在上皮细胞入侵过程中的细胞特征,特别关注其如何逃避自噬途径。