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Persistence of Intracellular Bacterial Pathogens—With a Focus on the Metabolic Perspective
Zitieren Sie bitte immer diese URN: urn:nbn:de:bvb:20-opus-222348
- Persistence has evolved as a potent survival strategy to overcome adverse environmental conditions. This capability is common to almost all bacteria, including all human bacterial pathogens and likely connected to chronic infections caused by some of these pathogens. Although the majority of a bacterial cell population will be killed by the particular stressors, like antibiotics, oxygen and nitrogen radicals, nutrient starvation and others, a varying subpopulation (termed persisters) will withstand the stress situation and will be able toPersistence has evolved as a potent survival strategy to overcome adverse environmental conditions. This capability is common to almost all bacteria, including all human bacterial pathogens and likely connected to chronic infections caused by some of these pathogens. Although the majority of a bacterial cell population will be killed by the particular stressors, like antibiotics, oxygen and nitrogen radicals, nutrient starvation and others, a varying subpopulation (termed persisters) will withstand the stress situation and will be able to revive once the stress is removed. Several factors and pathways have been identified in the past that apparently favor the formation of persistence, such as various toxin/antitoxin modules or stringent response together with the alarmone (p)ppGpp. However, persistence can occur stochastically in few cells even of stress-free bacterial populations. Growth of these cells could then be induced by the stress conditions. In this review, we focus on the persister formation of human intracellular bacterial pathogens, some of which belong to the most successful persister producers but lack some or even all of the assumed persistence-triggering factors and pathways. We propose a mechanism for the persister formation of these bacterial pathogens which is based on their specific intracellular bipartite metabolism. We postulate that this mode of metabolism ultimately leads, under certain starvation conditions, to the stalling of DNA replication initiation which may be causative for the persister state.…
Autor(en): | Wolfgang Eisenreich, Thomas Rudel, Jürgen Heesemann, Werner Goebel |
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URN: | urn:nbn:de:bvb:20-opus-222348 |
Dokumentart: | Artikel / Aufsatz in einer Zeitschrift |
Institute der Universität: | Fakultät für Biologie / Theodor-Boveri-Institut für Biowissenschaften |
Sprache der Veröffentlichung: | Englisch |
Titel des übergeordneten Werkes / der Zeitschrift (Englisch): | Frontiers in Cellular and Infection Microbiology |
ISSN: | 2235-2988 |
Erscheinungsjahr: | 2021 |
Band / Jahrgang: | 10 |
Aufsatznummer: | 615450 |
Originalveröffentlichung / Quelle: | Frontiers in Cellular and Infection Microbiology 2021, 10:615450. DOI: 10.3389/fcimb.2020.615450 |
DOI: | https://doi.org/10.3389/fcimb.2020.615450 |
Allgemeine fachliche Zuordnung (DDC-Klassifikation): | 5 Naturwissenschaften und Mathematik / 57 Biowissenschaften; Biologie / 570 Biowissenschaften; Biologie |
Freie Schlagwort(e): | ATP-DnaA complex; DNA replication initiation; intracellular bacterial pathogens; mechanisms of persister formation; persistence; stress conditions |
Datum der Freischaltung: | 01.02.2022 |
Lizenz (Deutsch): | CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International |