Programmed Cell Death in the Evolutionary Race against Bacterial Virulence Factors

Lacey, Carolyn A.; Miao, Edward A.

doi:10.1101/cshperspect.a036459

Cited by 33 publications

(23 citation statements)

References 187 publications

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“…We initially used 100:1 MOIs to evaluate programmed cell death in macrophages, but the realtime MOIs reached 10 3 to 10 4 after 6 h and 10 5 to 10 6 after 12 h of infection due to bacterial growth and macrophage death. Yersinia, Salmonella enterica, Enteropathogenic Escherichia coli, Listeria monocytogenes, and Francisella novicida infections may activate multiple cell death processes via PANoptosis that prevent pathogens from evading detection (Christgen et al, 2020;Lacey and Miao, 2020;Place et al, 2020). Paquette et al found that Yersinia inhibits TAK1 in infected mouse bone marrow macrophages (BMDMs), a feature that may help the bacteria to evade the host immune response (Paquette et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Real-Time Induction of Macrophage Apoptosis, Pyroptosis, and Necroptosis by Enterococcus faecalis OG1RF and Two Root Canal Isolated Strains

Chi

Lin

Meng

et al. 2021

Front. Cell. Infect. Microbiol.

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To investigate the effects of two Enterococcus faecalis root canal isolated strains (CA1 and CA2) and of the OG1RF strain on apoptosis, pyroptosis, and necroptosis in macrophages. The virulence factors of E. faecalis CA1 and CA2 pathogenic strains were annotated in the Virulence Factors Database (VFDB). E. faecalis CA1, CA2, and OG1RF strains were used to infect RAW264.7 macrophages (MOI, 100:1). We assessed the viability of intracellular and extracellular bacteria and of macrophages at 2, 6, and 12 h post-infection. We used a live cell imaging analysis system to obtain a dynamic curve of cell death after infection by each of the three E. faecalis strains. At 6 and 12 h post-infection, we quantified the mRNA expression levels of PANoptosis-related genes and proteins by RT-qPCR and western blot, respectively. We identified ultrastructural changes in RAW264.7 cells infected with E. faecalis OG1RF using transmission electron microscopy. We found 145 and 160 virulence factors in the CA1 and CA2 strains, respectively. The extracellular CA1 strains grew faster than the CA2 and OG1RF strains, and the amount of intracellular viable bacteria in the OG1RF group was highest at 6 and 12 h post-infection. The macrophages in the CA1 infection group were the first to reach the maximum PI-positivity in the cell death time point curve. We found the expressions of mRNA expression of caspase-1, GSDMD, caspase-3, MLKL, RIPK3, NLRP3, IL-1β and IL-18 and of proteins cleaved caspase-1, GSDMD, cleaved caspase-3 and pMIKL in the macrophages of the three infection groups to be upregulated (P<0.05). We detected ultrastructural changes of apoptosis, pyroptosis, and necroptosis in macrophages infected with E. faecalis. The three E. faecalis strains induced varying degrees of apoptosis, pyroptosis, and necroptosis that were probably associated with PANoptosis in macrophages. The E. faecalis CA1 strain exhibited faster growth and a higher real-time MOI, and it induced higher expression levels of some PANoptosis-related genes and proteins in the infected macrophages than the other strains tested.

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Section: Discussionmentioning

confidence: 99%

Real-Time Induction of Macrophage Apoptosis, Pyroptosis, and Necroptosis by Enterococcus faecalis OG1RF and Two Root Canal Isolated Strains

Chi

Lin

Meng

et al. 2021

Front. Cell. Infect. Microbiol.

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“…Conceptually, cell death appears to protect against most acute bacterial pathogens that infect hosts and, in many cases, even more successfully restricts non-pathogenic or opportunistic bacteria [ 19 , 20 ]. Earlier studies on cell death, before the identification of many of the key regulatory genes, suggested multiple forms of cell death are induced following infection with different bacterial pathogens [ 20 ]. Armed with the current understanding of the key molecules involved in different cell death pathways and how they are extensively interconnected, future research must carefully re-examine cell death during infections.…”

Section: Panoptosis In Bacterial Infectionmentioning

confidence: 99%

PANoptosis in microbial infection

Place

Lee

Kanneganti

2021

Current Opinion in Microbiology

156

114

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“…IL-1α and HMGB1) help promote inflammation, neutrophil recruitment and an adequate adaptive immune response (Mantovani, Dinarello, Molgora, & Garlanda, 2019), while pyroptosis eliminates intracellular bacterial replicative niches . The antibacterial function of inflammasomes is illustrated by the ability of various inflammasome sensor proteins to recognise and respond to bacterial ligands (Eldridge & Shenoy, 2015;Hayward et al, 2018), and the increased susceptibility to infection shown by mice with deletions in inflammasome components (Man, Karki, & Kanneganti, 2017;Lacey & Miao, 2019). Although inflammasomes have been best studied in myeloid cells, several inflammasome components, such as caspase-4/11 and pro-IL-18, are also expressed in IECs (Man, 2018;Winsor, Krustev, Bruce, Philpott, & Girardin, 2019).…”

Section: Signals For Inflammasome Activationmentioning

confidence: 99%

Vying for the control of inflammasomes: The cytosolic frontier of enteric bacterial pathogen–host interactions

Sanchez‐Garrido

Slater

Clements

et al. 2020

Cellular Microbiology

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Enteric pathogen–host interactions occur at multiple interfaces, including the intestinal epithelium and deeper organs of the immune system. Microbial ligands and activities are detected by host sensors that elicit a range of immune responses. Membrane‐bound toll‐like receptors and cytosolic inflammasome pathways are key signal transducers that trigger the production of pro‐inflammatory molecules, such as cytokines and chemokines, and regulate cell death in response to infection. In recent years, the inflammasomes have emerged as a key frontier in the tussle between bacterial pathogens and the host. Inflammasomes are complexes that activate caspase‐1 and are regulated by related caspases, such as caspase‐11, ‐4, ‐5 and ‐8. Importantly, enteric bacterial pathogens can actively engage or evade inflammasome signalling systems. Extracellular, vacuolar and cytosolic bacteria have developed divergent strategies to subvert inflammasomes. While some pathogens take advantage of inflammasome activation (e.g. Listeria monocytogenes, Helicobacter pylori), others (e.g. E. coli, Salmonella, Shigella, Yersinia sp.) deploy a range of virulence factors, mainly type 3 secretion system effectors, that subvert or inhibit inflammasomes. In this review we focus on inflammasome pathways and their immune functions, and discuss how enteric bacterial pathogens interact with them. These studies have not only shed light on inflammasome‐mediated immunity, but also the exciting area of mammalian cytosolic immune surveillance.

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Programmed Cell Death in the Evolutionary Race against Bacterial Virulence Factors

Cited by 33 publications

References 187 publications

Real-Time Induction of Macrophage Apoptosis, Pyroptosis, and Necroptosis by Enterococcus faecalis OG1RF and Two Root Canal Isolated Strains

Real-Time Induction of Macrophage Apoptosis, Pyroptosis, and Necroptosis by Enterococcus faecalis OG1RF and Two Root Canal Isolated Strains

PANoptosis in microbial infection

Vying for the control of inflammasomes: The cytosolic frontier of enteric bacterial pathogen–host interactions

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