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Microbial Modulation of Host Apoptosis and Pyroptosis

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889192809 Year: Pages: 109 DOI: 10.3389/978-2-88919-280-9 Language: English
Publisher: Frontiers Media SA
Subject: Internal medicine --- Science (General)
Added to DOAB on : 2015-12-10 11:59:06
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Infectious disease is the result of an interactive relationship between a microbial pathogen and its host. In this interaction both the host and the pathogen attempt to manipulate each other using a complex network to maximize their respective survival probabilities. Programmed host cell death is a direct outcome of host-pathogen interaction and may benefit host or pathogen depending on microbial pathogenesis. Apoptosis and pyroptosis are two common programmed cell death types induced by various microbial infections. Apoptosis is non-inflammatory programmed cell death and can be triggered through intrinsic or extrinsic pathways and with or without the contribution of mitochondria. Pyroptosis is an inflammatory cell death and is typically triggered by caspase-1 after its activation by various inflammasomes. However, some non-canonical caspase-1-independent proinflammatory cell death phenomena have been reported. Microbial pathogens are able to modulate host apoptosis and pyroptosis through different triggers and pathways. The promotion and inhibition of host apoptosis and pyroptosis vary and depend on the microbe types, virulence, and phenotypes. For example, virulent pathogens and attenuated vaccine strains may use different pathways to modulate host cell death. Specific microbial genes may be responsible for the modulation of host cell death. Different host cells, including macrophages, dendritic cells, and T cells, can undergo apoptosis and pyroptosis after microbial infections. The pathways of host apoptosis and pyroptosis induced by different microbes may also differ. Different methods can be used to study the interaction between microbes and host cell death system. The articles included in this E-book report the cutting edge findings in the areas of microbial modulation of host apoptosis, pyroptosis and inflammasome.

Endoplasmic reticulum - shape and function in stress translation

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193448 Year: Pages: 110 DOI: 10.3389/978-2-88919-344-8 Language: English
Publisher: Frontiers Media SA
Subject: Botany --- Science (General)
Added to DOAB on : 2016-03-10 08:14:32
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The endoplasmic reticulum (ER) is a manufacturing unit in eukaryotic cells required for the synthesis of proteins, lipids, metabolites and hormones. Besides supporting cellular signalling networks by its anabolic function, the ER on its own or in communication with other organelles directly initiates signalling processes of physiological significance. Based on the intimate and immediate involvement in stress signalling the ER is considered as sensory organelle on which cells strongly rely to effectively translate environmental cues into adaptive stress responses. The transcellular distribution of the ER providing comprehensive cell-to-cell connections in multicellular organisms probably allows a concerted action of cell alliances and tissue areas towards environmental constraints. At the cellular level, stress adaptation correlates with the capability of the ER machinery to synthesise proteins participating in stress signalling as well as in the activation of ER membrane localised proteins to start cell-protective signalling processes. Importantly, depending on the stress insult, the ER either supports protective strategies or initiates cell death programmes. Recent, genetic, molecular and cell biological studies have drawn an initial picture of underlying signalling events activated by ER membrane localised proteins. In this Research Topic, we provided a platform for articles describing research on ER morphology and metabolism with a focus on stress translation. The Research Topic is sub-divided into the following sections: 1. ER in stress signalling and adaptation 2. ER structure and biosynthetic functions 3. Regulation of protein processing 4. Regulation of programmed cell death

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