2021 journal article
TAK1 inhibition elicits mitochondrial ROS to block intracellular bacterial colonization
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 118(25).
author keywords: TAK1; ROS; mitochondria; intracellular bacteria
MeSH headings : Animals; Bacteria / growth & development; Caspase 3 / metabolism; Colony Count, Microbial; Hydrogen Sulfide / pharmacology; Intracellular Space / microbiology; MAP Kinase Kinase Kinases / antagonists & inhibitors; MAP Kinase Kinase Kinases / metabolism; Mice; Mitochondria / metabolism; Reactive Oxygen Species / metabolism; Receptor-Interacting Protein Serine-Threonine Kinases / metabolism; Salmonella / drug effects; Salmonella / growth & development; Yersinia / drug effects
TL;DR:
A previously unrecognized host defense mechanism is revealed, which is initiated by host recognition of pathogen-induced impairment in a host protein, TAK1, but not directly of pathogens.
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UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science)
Source: Web Of Science
Added: July 12, 2021
Significance We have found that bacterial inhibition of host TAK1 inflammatory signaling elicits an alternative host defense mechanism involving production of mitochondrial reactive oxygen species through caspase 8 and RIPK3. This finding allows a reinterpretation of mouse phenotypes harboring tissue-specific gene deletion of Tak1 , many of which die from tissue damage previously ascribed to impaired TAK1-dependent tissue homeostasis. We suggest that these phenotypes arise from misrecognition of compromised TAK1 as pathogen invasion.