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.
Highlights
Neisseria gonorrhoeae, known as gonococcus, is the causative agent of gonorrhea, a sexually transmitted infection that occurs exclusively in humans
N. gonorrhoeae is a major global public health concern due to its increasing resistance to antibiotics, which leads to the possibility of untreatable gonorrhea infections (World Health Organization [WHO], 2017; Rowley et al, 2019)
The recent studies of autophagy and N. gonorrhoeae infection show that in the early stages of invasion, bacteria survival is impaired by the autophagy pathway
Summary
Departamento de Genética, Ecologia e Evolução, Instituto de Ciencias Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. 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. 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), 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
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