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Taketomi, Y.

Publications and source records attributed to Taketomi, Y..

3 recordsLinked to original sources

Lysyl-phosphatidylglycerol promotes cell-to-cell interaction and biofilm formation of Staphylococcus aureus as a biofilm matrix component

Biofilms formed by Staphylococcus aureus contribute significantly to persistent infections and antibiotic resistance, driven by the unique composition of their extracellular matrix. While previous studies highlighted extracellular DNA, proteins, and polysaccharides as key components, the role of phospholipids in biofilm architecture remains underexplored. This study identifies extracellular phospholipids, including lysyl-phosphatidylglycerol (Lys-PG), phosphatidylglycerol, and cardiolipin (CL), as critical structural elements in S. aureus biofilms. Bacterial phospholipase A1 (PLA1) that cleaves the acyl ester bond at the sn-1 position of phospholipids effectively dispersed pre-formed biofilms and prevented new biofilm formation by hydrolyzing extracellular phospholipids, without affecting bacterial growth or exhibiting cytotoxicity. Microscopy analyses confirmed that PLA1 disrupts membranous nanostructures, including extracellular vesicles and nanofilaments, integral to biofilm stability. Lipidomic analysis revealed an enrichment of Lys-PG and CL in the biofilm matrix. Lys-PG promotes bacterial aggregation by acting as a molecular glue, mediated through electrostatic and hydrophobic interactions. Deletion of the mprF gene, responsible for Lys-PG synthesis, significantly impaired biofilm formation, confirming its essential role. These findings reveal a "moonlighting" function of phospholipids in biofilm architecture, providing insights into biofilm biology and presenting PLA1 as a promising tool for biofilm control. SignificanceBiofilms, dense bacterial communities, pose significant challenges across medical, industrial, and daily life contexts. Understanding their formation mechanisms is crucial for developing effective strategies against them. We investigated biofilm matrix components in S. aureus biofilms, focusing on phospholipids. Our study reveals the presence and significance of Lys-PG in the biofilm matrix, acting as a crucial factor in biofilm formation and maintenance. Through biochemical, lipidomic, and genetic analyses, we demonstrate the role of Lys-PG in facilitating cell-to-cell contacts, contributing to the robustness and thickness of S. aureus biofilms. These findings shed light on the physiological function of extracellular phospholipids in bacterial biofilms and suggest targeting Lys-PG and its synthetic mechanism as a promising strategy for biofilm control.

microbiology↗

Secreted phospholipase PLA2G12A-driven lysophospholipid signaling via lipolytic modification of extracellular vesicles facilitates pathogenic Th17 differentiation

Lipogenesis-driven metabolic flux is crucial for differentiation of pathogenic Th17 cells. Although our previous CRISPR-based screening identified PLA2G12A as a key player in this process, it has remained obscure how this secreted phospholipase A2 isoform controls Th17 differentiation. Here we show that global, T cell-specific, or fibroblast-specific deletion of PLA2G12A prevents Th17 differentiation and associated diseases including psoriasis and arthritis. PLA2G12A acts on Th17-derived extracellular vesicles (EVs) to produce lysophospholipids including the ROR{gamma}t activator 1-oleoyl-lysophosphatidylethanolamine. These lysophospholipids are further converted by autotaxin to lysophosphatidic acid (LPA), which assists Th17 differentiation mainly via LPA2 receptor. Moreover, PLA2G12A promotes the secretion and uptake of EVs by Th17 cells and alters their cargo contents. Defective Th17 differentiation by PLA2G12A deficiency is rescued by supplementation with PLA2G12A-modified EVs. Importantly, a PLA2G12A-blocking antibody prevents Th17 differentiation and ameliorates psoriasis and arthritis models. Thus, targeting the PLA2G12A-EV-lysophospholipid axis may be useful for treatment of Th17-related diseases.

immunology↗

Organism-Wide Analysis of Sepsis Reveals Mechanisms of Systemic Inflammation

Sepsis is a systemic response to infection with life-threatening consequences. Our understanding of the impact of sepsis across organs of the body is rudimentary. Here, using mouse models of sepsis, we generate a dynamic, organism-wide map of the pathogenesis of the disease, revealing the spatiotemporal patterns of the effects of sepsis across tissues. These data revealed two interorgan mechanisms key in sepsis. First, we discover a simplifying principle in the systemic behavior of the cytokine network during sepsis, whereby a hierarchical cytokine circuit arising from the pairwise effects of TNF plus IL-18, IFN-{gamma}, or IL-1{beta} explains half of all the cellular effects of sepsis on 195 cell types across 9 organs. Second, we find that the secreted phospholipase PLA2G5 mediates hemolysis in blood, contributing to organ failure during sepsis. These results provide fundamental insights to help build a unifying mechanistic framework for the pathophysiological effects of sepsis on the body.

immunology↗