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Epithelial Haven and Autophagy Breakout in Gonococci Infection.
Front Cell Dev Biol. 2020; 8:439.FC

Abstract

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 Neisseria gonorrhoeae, 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 N. gonorrhoeae. Its resistance to antibiotics has been increasing in the past few years, reducing the range of treatment options. N. gonorrhoeae requires a surface protein/receptor (Opa proteins, porin, Type IV pili, LOS) to adhere to and invade epithelial cells. During invasion and transcytosis, N. gonorrhoeae 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 N. gonorrhoeae during epithelial cell invasion, with a particular focus on how N. gonorrhoeae evades the autophagy pathway.

Authors+Show Affiliations

Departamento de Genética, Ecologia e Evolução, Instituto de Ciencias Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.Departamento de Genética, Ecologia e Evolução, Instituto de Ciencias Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.Departamento de Genética, Ecologia e Evolução, Instituto de Ciencias Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.Departamento de Genética, Ecologia e Evolução, Instituto de Ciencias Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

32582714

Citation

Mendes, Ana Clara, et al. "Epithelial Haven and Autophagy Breakout in Gonococci Infection." Frontiers in Cell and Developmental Biology, vol. 8, 2020, p. 439.
Mendes AC, Ciccone M, Gazolla B, et al. Epithelial Haven and Autophagy Breakout in Gonococci Infection. Front Cell Dev Biol. 2020;8:439.
Mendes, A. C., Ciccone, M., Gazolla, B., & Bahia, D. (2020). Epithelial Haven and Autophagy Breakout in Gonococci Infection. Frontiers in Cell and Developmental Biology, 8, 439. https://doi.org/10.3389/fcell.2020.00439
Mendes AC, et al. Epithelial Haven and Autophagy Breakout in Gonococci Infection. Front Cell Dev Biol. 2020;8:439. PubMed PMID: 32582714.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Epithelial Haven and Autophagy Breakout in Gonococci Infection. AU - Mendes,Ana Clara, AU - Ciccone,Marcone, AU - Gazolla,Bruna, AU - Bahia,Diana, Y1 - 2020/06/09/ PY - 2020/02/06/received PY - 2020/05/11/accepted PY - 2020/6/26/entrez PY - 2020/6/26/pubmed PY - 2020/6/26/medline KW - N. gonorrhoeae KW - autophagy KW - epithelial cell KW - epithelial cell invasion KW - intracellular pathogen SP - 439 EP - 439 JF - Frontiers in cell and developmental biology JO - Front Cell Dev Biol VL - 8 N2 - 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 Neisseria gonorrhoeae, 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 N. gonorrhoeae. Its resistance to antibiotics has been increasing in the past few years, reducing the range of treatment options. N. gonorrhoeae requires a surface protein/receptor (Opa proteins, porin, Type IV pili, LOS) to adhere to and invade epithelial cells. During invasion and transcytosis, N. gonorrhoeae 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 N. gonorrhoeae during epithelial cell invasion, with a particular focus on how N. gonorrhoeae evades the autophagy pathway. SN - 2296-634X UR - https://www.unboundmedicine.com/medline/citation/32582714/Epithelial_Haven_and_Autophagy_Breakout_in_Gonococci_Infection L2 - https://doi.org/10.3389/fcell.2020.00439 DB - PRIME DP - Unbound Medicine ER -
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