The development of tolerant and persister bacterial clinical pathogen cells (under stress conditions such as antimicrobials and environmental factors) is mediated by several molecular mechanisms, such as RpoS factor and other related general stress responses. Oxidant Tolerance Response (ROS) for instance, is produced as a natural response to the normal metabolism of oxygen and has important functions in cell signaling and homeostasis. Nevertheless, under environmental pressure (e.g., UV, heat, or drug exposure), ROS levels can rise and cause damage to the DNA, lipids, and proteins, which may lead to the death of the cell. Superoxide dismutase (SOD), catalase, and other antioxidant agents, such as glutathione and vitamin C, can eliminate ROS. When an imbalance between production and elimination of ROS occurs, with an increase of the former, cells are subjected to oxidative stress. Tau metabolism and cytochrome bd are part of the energy metabolism, the latest specifically by enhancing the tolerance of cells to oxidative stress (ROS response). Efflux pumps eliminate toxic elements and maintain the balance of compounds that are vital for bacterial survival. The bacterial SOS response which is related to DNA damage can be also considered an important mechanism of bacterial survival under stress conditions, and it is connected to other stress responses. Another important mechanism is Quorum Sensing/quenching (QS) network which allows cells to modify their collective behavior through signaling molecules, known as autoinducers, according to changes in the environment, and favors the formation of persister cells. Finally, one of the best-studied mechanisms of formation of persister cells involves the alarmone ppGpp.
This Research Topic is dedicated to increasing the understanding of the role of these molecular mechanisms in the survival of the bacterial clinical cell. To this end, we welcome manuscripts (reviews, mini-reviews and original articles) advancing the current knowledge on the main molecular mechanisms of tolerance and persistence in bacterial clinical strains, which are activated at the cell level in response to stress conditions both of antimicrobial and environmental origin. These molecular mechanisms include:
• General stress response (RpoS mediated);
• Reactive oxygen species (ROS) tolerance;
• Energy metabolism, including drug efflux pumps;
• Bacterial SOS response;
• Quorum sensing (QS) or bacterial communication;
• Guanosine tetraphosphate (ppGpp) and guanosine pentaphosphate (pppGpp) (p)ppGpp signaling
Furthermore, manuscripts describing the relationship between tolerance and persistence are welcome, as well as treatments against tolerant and persister bacterial clinical cells.
The development of tolerant and persister bacterial clinical pathogen cells (under stress conditions such as antimicrobials and environmental factors) is mediated by several molecular mechanisms, such as RpoS factor and other related general stress responses. Oxidant Tolerance Response (ROS) for instance, is produced as a natural response to the normal metabolism of oxygen and has important functions in cell signaling and homeostasis. Nevertheless, under environmental pressure (e.g., UV, heat, or drug exposure), ROS levels can rise and cause damage to the DNA, lipids, and proteins, which may lead to the death of the cell. Superoxide dismutase (SOD), catalase, and other antioxidant agents, such as glutathione and vitamin C, can eliminate ROS. When an imbalance between production and elimination of ROS occurs, with an increase of the former, cells are subjected to oxidative stress. Tau metabolism and cytochrome bd are part of the energy metabolism, the latest specifically by enhancing the tolerance of cells to oxidative stress (ROS response). Efflux pumps eliminate toxic elements and maintain the balance of compounds that are vital for bacterial survival. The bacterial SOS response which is related to DNA damage can be also considered an important mechanism of bacterial survival under stress conditions, and it is connected to other stress responses. Another important mechanism is Quorum Sensing/quenching (QS) network which allows cells to modify their collective behavior through signaling molecules, known as autoinducers, according to changes in the environment, and favors the formation of persister cells. Finally, one of the best-studied mechanisms of formation of persister cells involves the alarmone ppGpp.
This Research Topic is dedicated to increasing the understanding of the role of these molecular mechanisms in the survival of the bacterial clinical cell. To this end, we welcome manuscripts (reviews, mini-reviews and original articles) advancing the current knowledge on the main molecular mechanisms of tolerance and persistence in bacterial clinical strains, which are activated at the cell level in response to stress conditions both of antimicrobial and environmental origin. These molecular mechanisms include:
• General stress response (RpoS mediated);
• Reactive oxygen species (ROS) tolerance;
• Energy metabolism, including drug efflux pumps;
• Bacterial SOS response;
• Quorum sensing (QS) or bacterial communication;
• Guanosine tetraphosphate (ppGpp) and guanosine pentaphosphate (pppGpp) (p)ppGpp signaling
Furthermore, manuscripts describing the relationship between tolerance and persistence are welcome, as well as treatments against tolerant and persister bacterial clinical cells.
