Lounging in a lysosome: the intracellular lifestyle of Coxiella burnetii.
Daniel E. Voth,Robert A. Heinzen +1 more
TLDR
Current understanding of the cellular events that occur during parasitism of host cells by Coxiella, including deployment of a type IV secretion system to deliver effector proteins to the host cytosol is summarized.Abstract:
Summary
Most intracellular parasites employ sophisticated mechanisms to direct biogenesis of a vacuolar replicative niche that circumvents default maturation through the endolysosomal cascade. However, this is not the case of the Q fever bacterium, Coxiella burnetii. This hardy, obligate intracellular pathogen has evolved to not only survive, but to thrive, in the harshest of intracellular compartments: the phagolysosome. Following internalization, the nascent Coxiella phagosome ultimately develops into a large and spacious parasitophorous vacuole (PV) that acquires lysosomal characteristics such as acidic pH, acid hydrolases and cationic peptides, defences designed to rid the host of intruders. However, transit of Coxiella to this environment is initially stalled, a process that is apparently modulated by interactions with the autophagic pathway. Coxiella actively participates in biogenesis of its PV by synthesizing proteins that mediate phagosome stalling, autophagic interactions, and development and maintenance of the mature vacuole. Among the potential mechanisms mediating these processes is deployment of a type IV secretion system to deliver effector proteins to the host cytosol. Here we summarize our current understanding of the cellular events that occur during parasitism of host cells by Coxiella.read more
Citations
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Nuclear trafficking of the anti‐apoptotic Coxiella burnetii effector protein AnkG requires binding to p32 and Importin‐α1
Walter Schäfer,Rita A. Eckart,Benedikt Schmid,Hasret Cagköylü,Kerstin Hof,Yves A. Muller,Bushra Amin,Anja Lührmann +7 more
TL;DR: The obligate intracellular bacterium Coxiella burnetii causes the zoonotic disease Q‐fever and the T4SS effector AnkG inhibits pathogen‐induced host cell apoptosis, which is believed to be important for the establishment of a persistent infection.
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Galectin‐3 disruption impaired tumoral angiogenesis by reducing VEGF secretion from TGFβ1‐induced macrophages
Camila Maria Longo Machado,Luciana N ogueira Sousa Andrade,Verônica R. Teixeira,Fabricio F. Costa,Camila Maria de Melo,Sofia Nascimento dos Santos,Suely Nonogaki,Fu-Tong Liu,Emerson Soares Bernardes,Anamaria A ranha Camargo,Roger Chammas +10 more
TL;DR: It is reported that galectin‐3 disruption in tumor stroma and parenchyma decreases angiogenesis through interfering with the responses of macrophages to the interdependent VEGF and TGFβ1 signaling pathways.
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Organ‐Specific Responses of Vacuolar H+‐ATPase in the Shoots and Roots of C3 Halophyte Suaeda salsa to NaCl
TL;DR: It is suggested that the tissue-specific characteristics of V-ATPase were related to the different patterns of growth and ion accumulation in shoots and roots of S. salsa.
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Leptin in the regulation of the immunometabolism of adipose tissue-macrophages.
Lauar de Brito Monteiro,Jessica Aparecida da Silva Pereira,Jessica Aparecida da Silva Pereira,Lohanna Palhinha,Pedro M. Moraes-Vieira,Pedro M. Moraes-Vieira +5 more
TL;DR: The immunometabolic effects of leptin in Mϕs are discussed and how hyperleptinemia can contribute to the low‐grade systemic inflammation in obesity.
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Connective tissue growth factor/CCN2 stimulates actin disassembly through Akt/protein kinase B-mediated phosphorylation and cytoplasmic translocation of p27Kip-1
TL;DR: The role of CTGF in cell migration and actin disassembly in human mesangial cells is delineated and the proposed role of p27Kip‐1 as a mediator of actin rearrangement is sheds new light on.
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