Sepsis-induced arrhythmia, linked to sudden cardiac death, is associated with gut microbiota, though the exact relationship is unclear. This study aimed to elucidate the relationship between () and arrhythmia. The relative abundance of was increased in cecal ligation and puncture (CLP)-induced septic mice. Live , supernatant, and outer membrane vesicles (OMVs) resulted in premature ventricular beat (PVB), sinus arrhythmia (SA), and increased arrhythmia and mortality in sepsis model through dysregulated ion channel proteins. Moreover, short-chain fatty acids (SCFAs) showed antibacterial effects . We confirmed sodium acetate (C2) and sodium butyrate (C4) protect from -induced arrhythmia, and C2 and C4 protected from septic arrhythmia by activating free fatty acid receptor 2 and 3 (FFAR2 and FFAR3) in mice. These findings point to how 's OMVs trigger arrhythmia, and SCFAs may be a treatment for septic arrhythmia.
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http://dx.doi.org/10.1016/j.isci.2024.110572 | DOI Listing |
J Nanobiotechnology
January 2025
Stomatological Hospital, School of Stomatology, Southern Medical University, Guangzhou, Guangdong, China.
Extracellular vesicles (EVs) are membrane-bound vesicles that are shed or secreted from the cell membrane and enveloped by a lipid bilayer. They possess stability, low immunogenicity, and non-cytotoxicity, exhibiting extensive prospects in regenerative medicine (RM). However, natural EVs pose challenges, such as insufficient targeting capabilities, potential biosafety concerns, and limited acquisition pathways.
View Article and Find Full Text PDFNat Cell Biol
January 2025
Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA, USA.
Outer mitochondrial membrane (OMM) proteins communicate with the cytosol and other organelles, including the endoplasmic reticulum. This communication is important in thermogenic adipocytes to increase the energy expenditure that controls body temperature and weight. However, the regulatory mechanisms of OMM protein insertion are poorly understood.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
VIB-UGent Center for Inflammation Research, Ghent, Belgium.
Background: The brain is shielded from the peripheral circulation by central nervous system (CNS) barriers, comprising the well-known blood-brain barrier (BBB) and the less recognized blood-cerebrospinal fluid (CSF) barrier located within the brain ventricles. The gut microbiota represents a diverse and dynamic population of microorganisms that can influence the health of the host, including the development of neurological disorders like Alzheimer's disease (AD). However, the intricate mechanisms governing the interplay between the gut and brain remain elusive, and the means by which gut-derived signals traverse the CNS barriers remain unclear.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Michigan State University, Grand Rapids, MI, USA.
Background: The pathological correlate most tightly associated with cognitive decline in AD is synapse loss. The presence of pathological tau significantly correlates with synaptotoxicity and cognitive decline in AD, yet it is currently unclear how pathological tau causes synapse loss. Within the brain, complement component C1q coats the outer membrane of weak or damaged synapses, resulting in the phagocytic removal of tagged synapses by microglia.
View Article and Find Full Text PDFFront Microbiol
December 2024
Umeå Centre for Microbial Research (UCMR), Umeå University, Umeå, Sweden.
Lipoproteins are crucial for maintaining the structural integrity of bacterial membranes. In Gram-negative bacteria, the localization of lipoprotein (Lol) system facilitates the transport of these proteins from the inner membrane to the outer membrane. In , an ε-proteobacterium, lipoprotein transport differs significantly from the canonical and well-studied system in , particularly due to the absence of LolB and the use of a LolF homodimer instead of the LolCE heterodimer.
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