Listeria monocytogenes is an intracellular facultative bacterial pathogen that remains a global challenge to food production and public health, due to its strong association with foodborne transmission and relatively high mortality burden in clinical infection cases. This pathogen can well-adapt to various stress environments and replicate in animal cells as well as in external environment. The move from stress environments to the cytosol requires the interplay of L. monocytogenes factors that promote survival in the gut, bacterial invasion, and phagosomal escape, followed by replication and movement within the cytosol and spread to adjacent cells.
Listeria has evolved many sophisticated mechanisms to facilitate its transition from saprophyte to cytosolic pathogen, and more importantly, to evade the host immune defense system to survive in host cells. As the “smart” intracellular bacteria, Listeria employs different strategies to hijack host cell biology, ranging from changes in organelle morphology to effects on host signaling pathways via bacterial virulence factors. However, during the transition from environmental adaption to host infection, many critical questions about how L. monocytogenes establishes and maintains a productive infection, as well as the complexity of molecular basis involved in host-pathogen interactions, remain to be fully understood.
Listeria monocytogenes has many regulatory and virulence-associated factors that constitute the complex mechanisms of regulation and diverse responses to stress, allowing it to survive in highly distinct environmental conditions and to switch from saprophytism to virulence. Many factors have been identified yet, such as LLO, PrfA, ActA, and SigB; however, novel factors remain to be explored and further investigated. We also lack in-depth knowledge of how these factors regulate transition of this bacterium from environmental adaption to host infection. Importantly, it is also critical to better understand how Listeria evades host defenses by modulating the innate immunity and the adaptive immunity, which in turn can make Listeria become an attractive antigen-delivering vaccine for cancer immunotherapy.
This Research Topic aims to collect Original Research articles and Reviews about the stress and infection biology field of Listeria, including themes about bacterial physiology and regulation, host immune responses against Listeria infection, and Listeria-host interactions.
- Theme 1: Regulation of effectors by Listeria during transition from environmental adaption to host infection
- Theme 2: New insights into virulence regulators and identification of the yet unknown virulence factors
- Theme 3: Molecular mechanisms of Listeria-host interactions during infection
- Theme 4: Listeria evasion of and modulation on host immune defenses
Listeria monocytogenes is an intracellular facultative bacterial pathogen that remains a global challenge to food production and public health, due to its strong association with foodborne transmission and relatively high mortality burden in clinical infection cases. This pathogen can well-adapt to various stress environments and replicate in animal cells as well as in external environment. The move from stress environments to the cytosol requires the interplay of L. monocytogenes factors that promote survival in the gut, bacterial invasion, and phagosomal escape, followed by replication and movement within the cytosol and spread to adjacent cells.
Listeria has evolved many sophisticated mechanisms to facilitate its transition from saprophyte to cytosolic pathogen, and more importantly, to evade the host immune defense system to survive in host cells. As the “smart” intracellular bacteria, Listeria employs different strategies to hijack host cell biology, ranging from changes in organelle morphology to effects on host signaling pathways via bacterial virulence factors. However, during the transition from environmental adaption to host infection, many critical questions about how L. monocytogenes establishes and maintains a productive infection, as well as the complexity of molecular basis involved in host-pathogen interactions, remain to be fully understood.
Listeria monocytogenes has many regulatory and virulence-associated factors that constitute the complex mechanisms of regulation and diverse responses to stress, allowing it to survive in highly distinct environmental conditions and to switch from saprophytism to virulence. Many factors have been identified yet, such as LLO, PrfA, ActA, and SigB; however, novel factors remain to be explored and further investigated. We also lack in-depth knowledge of how these factors regulate transition of this bacterium from environmental adaption to host infection. Importantly, it is also critical to better understand how Listeria evades host defenses by modulating the innate immunity and the adaptive immunity, which in turn can make Listeria become an attractive antigen-delivering vaccine for cancer immunotherapy.
This Research Topic aims to collect Original Research articles and Reviews about the stress and infection biology field of Listeria, including themes about bacterial physiology and regulation, host immune responses against Listeria infection, and Listeria-host interactions.
- Theme 1: Regulation of effectors by Listeria during transition from environmental adaption to host infection
- Theme 2: New insights into virulence regulators and identification of the yet unknown virulence factors
- Theme 3: Molecular mechanisms of Listeria-host interactions during infection
- Theme 4: Listeria evasion of and modulation on host immune defenses
