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Kyle Caution

Researcher at Ohio State University

Publications -  24
Citations -  1090

Kyle Caution is an academic researcher from Ohio State University. The author has contributed to research in topics: Autophagy & Burkholderia cenocepacia. The author has an hindex of 16, co-authored 22 publications receiving 912 citations.

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Autophagy stimulation by rapamycin suppresses lung inflammation and infection by Burkholderia cenocepacia in a model of cystic fibrosis.

TL;DR: It is shown for the first time that in wild-type macrophages, many B. cepacia reside in autophagosomes that fuse with lysosomes at later stages of infection, and it is demonstrated that if efficiently activated, autophagy can control B. Cepacia infection and ameliorate the associated inflammation.
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Caspase-11 promotes the fusion of phagosomes harboring pathogenic bacteria with lysosomes by modulating actin polymerization.

TL;DR: Caspase-11 was dispensable for the fusion of lysosomes with phagosomes containing nonpathogenic bacteria, uncovering a fundamental difference in the trafficking of phagosome according to their cargo.
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Aging is associated with hypermethylation of autophagy genes in macrophages

TL;DR: This study builds a foundation for the development of novel therapeutics aimed to improve autophagy in the elderly population and suggests a role for DNMT2 in DNA methylation activities.
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Apoptosis-associated Speck-like Protein (ASC) Controls Legionella pneumophila Infection in Human Monocytes

TL;DR: The data demonstrate that L. pneumophila manipulates ASC levels to evade inflammasome activation and grow in human monocytes by targeting ASC, which modulates the inflammaome, the apoptosome, and NF-κB pathway simultaneously.
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Depletion of the Ubiquitin-binding Adaptor Molecule SQSTM1/p62 from Macrophages Harboring cftr ΔF508 Mutation Improves the Delivery of Burkholderia cenocepacia to the Autophagic Machinery

TL;DR: Interestingly, the depletion of p62 from ΔF508 macrophages results in the release of the autophagy molecule beclin1 (BECN1) from the mutant CFTR aggregates and allows its redistribution and recruitment to the B. cepacia vacuole, mediating the acquisition of theAutophagy marker LC3 and bacterial clearance via Autophagy.