About this Research Topic
Brucella is a Gram-negative bacteria that infects humans and many kinds of domestic animals, and is capable of causing brucellosis, a chronic febrile infectious disease. With severe damage to the reproductive system and joints of humans and livestock, Brucella causes great harm to the development of animal husbandry and human health.
The main hosts of Brucella are cattle, sheep and pigs. Brucellosis can also be transferred from animals to humans, and human-to-human transmission has been reported. Brucella invades the human body through the damaged skin, digestive tract, respiratory mucosa, eye conjunctiva and sexual organ mucosa. It was reported that Brucella could survive and proliferate in both phagocytes and non-phagocytic cells of the host. In the past years, the mechanism of Brucella intracellular survival has attracted much attention, and we have gained a great deal of knowledge in this regard. Smooth-type Brucella is internalized into cells by phagocytosis through lipid rafts, in which LPS O-chain polysaccharide is a key factor. Upon entry into the cell, Brucella undergoes a complex multi-stage intracellular transformation from the Brucella-containing vacuoles (BCVs) to replicative endosome-like vacuoles (rBCVs) that allow bacteria to replicate in large numbers, in which Type IV secretion system (T4SS) effector proteins play a significant role, mediating the interaction between BCV and endoplasmic reticulum. Additionally, rBCVs will further mature into autophagic BCVs (aBCVs) with lysosomal characteristics, which establishes the basis for cell-to-cell transmission of Brucella. Finally, the bacteria spread to placental trophoblast cells, the genital tract and the mononuclear phagocyte system, establishing persistent and chronic infection in the host. Even though there have been extensive efforts, the facultative intracellular survival mechanisms of Brucella have not been fully described. It is worth further exploring the specific mechanisms, which provides a theoretical basis for the pathogenesis, prevention and therapy of brucellosis.
In this Research Topic, we focus on the intracellular survival mechanisms of Brucella and the pathogenesis and epidemiology of brucellosis, aiming to explore preventive and therapeutic strategies, including safer and more effective Brucella vaccines.
We welcome submissions of all types of articles (Original Research, Methods, Opinion, Review, Mini-Review, Perspective, and Hypothesis & Theory) focusing on the Brucella, including but not limited to the following subtopics:
1. Research on mechanisms of Brucella intracellular survival within host cells.
2. Exploring chronic infection mechanisms of Brucella by using multi-omics, CRISPR, etc.
3. Investigation of the epidemiology of brucellosis.
4. Studies on vaccines for brucellosis (inactivated, mutant-derived, live-attenuated, and novel target).
The main hosts of Brucella are cattle, sheep and pigs. Brucellosis can also be transferred from animals to humans, and human-to-human transmission has been reported. Brucella invades the human body through the damaged skin, digestive tract, respiratory mucosa, eye conjunctiva and sexual organ mucosa. It was reported that Brucella could survive and proliferate in both phagocytes and non-phagocytic cells of the host. In the past years, the mechanism of Brucella intracellular survival has attracted much attention, and we have gained a great deal of knowledge in this regard. Smooth-type Brucella is internalized into cells by phagocytosis through lipid rafts, in which LPS O-chain polysaccharide is a key factor. Upon entry into the cell, Brucella undergoes a complex multi-stage intracellular transformation from the Brucella-containing vacuoles (BCVs) to replicative endosome-like vacuoles (rBCVs) that allow bacteria to replicate in large numbers, in which Type IV secretion system (T4SS) effector proteins play a significant role, mediating the interaction between BCV and endoplasmic reticulum. Additionally, rBCVs will further mature into autophagic BCVs (aBCVs) with lysosomal characteristics, which establishes the basis for cell-to-cell transmission of Brucella. Finally, the bacteria spread to placental trophoblast cells, the genital tract and the mononuclear phagocyte system, establishing persistent and chronic infection in the host. Even though there have been extensive efforts, the facultative intracellular survival mechanisms of Brucella have not been fully described. It is worth further exploring the specific mechanisms, which provides a theoretical basis for the pathogenesis, prevention and therapy of brucellosis.
In this Research Topic, we focus on the intracellular survival mechanisms of Brucella and the pathogenesis and epidemiology of brucellosis, aiming to explore preventive and therapeutic strategies, including safer and more effective Brucella vaccines.
We welcome submissions of all types of articles (Original Research, Methods, Opinion, Review, Mini-Review, Perspective, and Hypothesis & Theory) focusing on the Brucella, including but not limited to the following subtopics:
1. Research on mechanisms of Brucella intracellular survival within host cells.
2. Exploring chronic infection mechanisms of Brucella by using multi-omics, CRISPR, etc.
3. Investigation of the epidemiology of brucellosis.
4. Studies on vaccines for brucellosis (inactivated, mutant-derived, live-attenuated, and novel target).
Keywords: brucellosis, Intracellular survival, chronic infection, Brucella vaccine, epidemiology
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