Host organisms often undergo programmed cell death (PCD) after microbial infections. Commonly observed programmed cell death types include apoptosis, pyroptosis, autophagy, and necroptosis. Apoptosis is typically considered to be a non-inflammatory form of programmed cell death and can be triggered through intrinsic or extrinsic pathways; with or without the contribution of mitochondria. Pyroptosis is an inflammatory cell death and is typically triggered by caspase-1 or caspase-11 downstream of various inflammasomes. Autophagy-induced PCD is associated with the appearance of autophagosomes and depends on autophagy proteins. Necroptosis is a programmed form of necrosis that is initiated by tumor necrosis factor (TNF) and its cognate receptor TNFR1 or Toll-like receptor (TLR) signaling. These types of PCD can all be induced by microbial infection.
Meanwhile, microbes modulate host PCD through different triggers, pathways, and strategies. The promotion or inhibition of host PCD depends on the microbe types, virulence factors, genetic variation, and microbial phenotypes. For example, virulent wild type Brucella usually prevents macrophage cell death, while attenuated Brucella mutants, including many vaccine strains, trigger macrophage PCD. Many microbial proteins (e.g., Yersinia YopJ and YopK) can induce or inhibit host cell death. Different host cells, such as macrophages, dendritic cells, and T cells, can undergo different types of PCD in response to the same pathogen. How different microbes or microbial proteins affect host PCD outcomes is complex and still remain largely unclear.
As an outcome of host-pathogen interactions programmed host cell death may benefit the host or pathogen, depending on the pathogenesis of the microbe and host immunity. Much progress has been made in the field in recent years with new methods and intensive studies. This Frontiers Research Topic focuses on the exciting research investigating microbial modulation of host programmed cell death. This Topic is a follow-up to the Research Topic, “Microbial modulation of host apoptosis and pyroptosis” (https://www.frontiersin.org/research-topics/1309/microbial-modulation-of-host-apoptosis-and-pyroptosis).
This new Research Topic, in addition to apoptosis and pyroptosis, will also encompass other forms of cell death, including autophagy and necroptosis, that are now known to also occur in the context of host-pathogen interactions. An integrative and systematic collection of research articles in this domain will allow us to share and examine and the new progress in this important area of research and support a better understanding of the intricate mechanisms underlying host-pathogen interactions.
Host organisms often undergo programmed cell death (PCD) after microbial infections. Commonly observed programmed cell death types include apoptosis, pyroptosis, autophagy, and necroptosis. Apoptosis is typically considered to be a non-inflammatory form of programmed cell death and can be triggered through intrinsic or extrinsic pathways; with or without the contribution of mitochondria. Pyroptosis is an inflammatory cell death and is typically triggered by caspase-1 or caspase-11 downstream of various inflammasomes. Autophagy-induced PCD is associated with the appearance of autophagosomes and depends on autophagy proteins. Necroptosis is a programmed form of necrosis that is initiated by tumor necrosis factor (TNF) and its cognate receptor TNFR1 or Toll-like receptor (TLR) signaling. These types of PCD can all be induced by microbial infection.
Meanwhile, microbes modulate host PCD through different triggers, pathways, and strategies. The promotion or inhibition of host PCD depends on the microbe types, virulence factors, genetic variation, and microbial phenotypes. For example, virulent wild type Brucella usually prevents macrophage cell death, while attenuated Brucella mutants, including many vaccine strains, trigger macrophage PCD. Many microbial proteins (e.g., Yersinia YopJ and YopK) can induce or inhibit host cell death. Different host cells, such as macrophages, dendritic cells, and T cells, can undergo different types of PCD in response to the same pathogen. How different microbes or microbial proteins affect host PCD outcomes is complex and still remain largely unclear.
As an outcome of host-pathogen interactions programmed host cell death may benefit the host or pathogen, depending on the pathogenesis of the microbe and host immunity. Much progress has been made in the field in recent years with new methods and intensive studies. This Frontiers Research Topic focuses on the exciting research investigating microbial modulation of host programmed cell death. This Topic is a follow-up to the Research Topic, “Microbial modulation of host apoptosis and pyroptosis” (https://www.frontiersin.org/research-topics/1309/microbial-modulation-of-host-apoptosis-and-pyroptosis).
This new Research Topic, in addition to apoptosis and pyroptosis, will also encompass other forms of cell death, including autophagy and necroptosis, that are now known to also occur in the context of host-pathogen interactions. An integrative and systematic collection of research articles in this domain will allow us to share and examine and the new progress in this important area of research and support a better understanding of the intricate mechanisms underlying host-pathogen interactions.