Pyroptosis in defense against intracellular bacteria.

Autophagy Environmental pathogen Guanylate-binding protein Host-adapted pathogen Intracellular bacteria Pyroptosis

Journal

Seminars in immunology
ISSN: 1096-3618
Titre abrégé: Semin Immunol
Pays: England
ID NLM: 9009458

Informations de publication

Date de publication:
09 2023
Historique:
received: 12 05 2023
revised: 29 06 2023
accepted: 03 07 2023
pmc-release: 01 09 2024
medline: 21 8 2023
pubmed: 11 7 2023
entrez: 10 7 2023
Statut: ppublish

Résumé

Pathogenic microbes invade the human body and trigger a host immune response to defend against the infection. In response, host-adapted pathogens employ numerous virulence strategies to overcome host defense mechanisms. As a result, the interaction between the host and pathogen is a dynamic process that shapes the evolution of the host's immune response. Among the immune responses against intracellular bacteria, pyroptosis, a lytic form of cell death, is a crucial mechanism that eliminates replicative niches for intracellular pathogens and modulates the immune system by releasing danger signals. This review focuses on the role of pyroptosis in combating intracellular bacterial infection. We examine the cell type specific roles of pyroptosis in neutrophils and intestinal epithelial cells. We discuss the regulatory mechanisms of pyroptosis, including its modulation by autophagy and interferon-inducible GTPases. Furthermore, we highlight that while host-adapted pathogens can often subvert pyroptosis, environmental microbes are effectively eliminated by pyroptosis.

Identifiants

pubmed: 37429234
pii: S1044-5323(23)00096-9
doi: 10.1016/j.smim.2023.101805
pmc: PMC10530505
mid: NIHMS1917842
pii:
doi:

Types de publication

Journal Article Review Research Support, Non-U.S. Gov't Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

101805

Subventions

Organisme : NIAID NIH HHS
ID : R01 AI133236
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR072694
Pays : United States
Organisme : NIAID NIH HHS
ID : R56 AI139425
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI148243
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI175078
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI139425
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI103197
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI139304
Pays : United States
Organisme : NIAID NIH HHS
ID : R56 AI133236
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI136920
Pays : United States

Informations de copyright

Copyright © 2023 Elsevier Ltd. All rights reserved.

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Auteurs

Lupeng Li (L)

Department of Integrative Immunobiology, Duke University School of Medicine, Durham, NC, USA; Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC, USA; Department of Cell Biology, Duke University School of Medicine, Durham, NC, USA; Department of Pathology, Duke University School of Medicine, Durham, NC, USA.

Mary S Dickinson (MS)

Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC, USA.

Jörn Coers (J)

Department of Integrative Immunobiology, Duke University School of Medicine, Durham, NC, USA; Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC, USA.

Edward A Miao (EA)

Department of Integrative Immunobiology, Duke University School of Medicine, Durham, NC, USA; Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC, USA; Department of Cell Biology, Duke University School of Medicine, Durham, NC, USA; Department of Pathology, Duke University School of Medicine, Durham, NC, USA. Electronic address: edward.miao@duke.edu.

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