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http://dx.doi.org/10.1042/bst0270487 | DOI Listing |
PeerJ
January 2025
Department of Medical Microbiology and Infection Prevention, Amsterdam University Medical Centers, Amsterdam, Netherlands.
Background: The initial colonization of the infant gut is a complex process that defines the foundation for a healthy microbiome development. is one of the first colonizers of newborns' gut, playing a crucial role in the healthy development of both the host and its microbiome. However, exhibits significant genomic diversity, with subspecies ( subsp.
View Article and Find Full Text PDFGut Microbes
December 2025
Microbiome-Host Interactions, Institut Pasteur, Université Paris Cité, INSERM U1306, CNRS UMR6047, Paris, France.
Metabolic syndrome is, in humans, associated with alterations in the composition and localization of the intestinal microbiota, including encroachment of bacteria within the colon's inner mucus layer. Possible promoters of these events include dietary emulsifiers, such as carboxymethylcellulose (CMC) and polysorbate-80 (P80), which, in mice, result in altered microbiota composition, encroachment, low-grade inflammation and metabolic syndrome. While assessments of gut microbiota composition have largely focused on fecal/luminal samples, we hypothesize an outsized role for changes in mucus microbiota in driving low-grade inflammation and its consequences.
View Article and Find Full Text PDFJ Biol Chem
January 2025
Division of Regulatory Glycobiology, Graduate School of Pharmaceutical Sciences, Tohoku Medical and Pharmaceutical University; Institute of Molecular Biomembrane and Glycobiology, Tohoku Medical and Pharmaceutical University, 4-4-1 Komatsushima, Aoba-ku, Sendai, Miyagi 981-8558, Japan. Electronic address:
Core fucosylation is one of the most essential modifications of the N-glycans, catalyzed by α1,6-fucosyltransferase (Fut8), which transfers fucose from guanosine 5'-diphosphate (GDP)-fucose to the innermost N-acetylglucosamine residue of N-glycans in an α1-6 linkage. Our previous studies demonstrated that lipopolysaccharide (LPS) can induce a more robust neuroinflammatory response in Fut8 homozygous knockout (KO) (Fut8) and heterozygous KO (Fut8) mice contrasted to the wild-type (Fut8) mice. Exogenous administration of L-fucose suppressed LPS-induced neuroinflammation.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Gastroenterology and Hepatology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
There are limited studies on the improvement of leaky gut with minor inflammation associated with various diseases. To explore the therapeutic potential of Lactiplantibacillus plantarum 22 A-3, a member of the Lactobacillus species, in addressing a leaky gut. Lactiplantibacillus plantarum 22 A-3 was administered to a leaky gut mice model with low dextran sulfate sodium concentrations.
View Article and Find Full Text PDFInflamm Res
January 2025
Department of Pathology and Laboratory Medicine, Medical University of South Carolina, 173 Ashley Ave, Charleston, SC, 29425, USA.
Background: Sepsis-associated encephalopathy (SAE) often results from neuroinflammation. Recent studies have shown that brain platelet-derived growth factor receptor β (PDGFRβ) cells, including pericytes, may act as early sensors of infection by secreting monocyte chemoattractant protein-1 (MCP-1), which transmits inflammatory signals to the central nervous system. The erythroblast transformation-specific (ETS) transcription factor Friend leukemia virus integration 1 (Fli-1) plays a critical role in inflammation by regulating the expression of key cytokines, including MCP-1.
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