8 results match your criteria: "Max Planck Institute of Epigenetics and Immunobiology[Affiliation]"
Metabolic and functional remodeling of colonic macrophages in response to high-fat diet-induced obesity.
iScience
October 2023
Department of Immunology, University of Sao Paulo, Sao Paulo, Brazil.
Article Synopsis
- Research shows that high-fat diets lead to obesity and increased macrophage infiltration in the colon, impacting their function and metabolism.
- Resident colonic macrophages exhibit a lipid metabolism signature similar to lipid-associated macrophages, with a specific sub-cluster identified through single-cell RNA sequencing.
- These macrophages show improved phagocytic capacity and fewer lipid droplets compared to those in lean mice, suggesting they adapt to limit bacterial translocation in response to high-fat diets.
Leptin Signaling Suppression in Macrophages Improves Immunometabolic Outcomes in Obesity.
Diabetes
July 2022
Laboratory of Immunometabolism, Department of Genetics, Evolution, Microbiology and Immunology, University of Campinas, Campinas, Brazil.
Article Synopsis
- Obesity leads to low-grade inflammation, increasing the risk of insulin resistance, with leptin being a key player by regulating food intake and being elevated in obese individuals.
- Leptin enhances macrophage responses to inflammation, promoting cytokine production and changes in mitochondrial function, thereby intensifying the inflammatory response.
- Intervening in leptin signaling pathways may offer new strategies for treating obesity-related inflammation and improving insulin resistance.
Mitochondrial metabolism coordinates stage-specific repair processes in macrophages during wound healing.
Cell Metab
December 2021
Department of Dermatology, University of Cologne, 50937 Cologne, Germany; Center for Molecular Medicine Cologne (CMMC), University of Cologne, 50931 Cologne, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50674 Cologne, Germany; Institute of Zoology, Developmental Biology Unit, University of Cologne, 50674 Cologne, Germany. Electronic address:
Article Synopsis
- - Wound healing involves a shift in the role of macrophages from promoting inflammation to facilitating resolution, with changes in their metabolism playing a crucial role.
- - Researchers studied macrophages at different stages of skin wound healing in mice, discovering that early-stage macrophages rely on mitochondrial ROS production for effective repair, while late-stage macrophages depend on different pathways for resolution.
- - The findings highlight that alterations in mitochondrial metabolism are vital for regulating macrophage functions throughout the wound healing process, marking it as an essential factor for timely recovery.
Opa1 relies on cristae preservation and ATP synthase to curtail reactive oxygen species accumulation in mitochondria.
Redox Biol
May 2021
Veneto Institute of Molecular Medicine, Padova, Italy; Department of Biology, University of Padova, Padova, Italy. Electronic address:
Reactive oxygen species (ROS) are a common product of active mitochondrial respiration carried in mitochondrial cristae, but whether cristae shape influences ROS levels is unclear. Here we report that the mitochondrial fusion and cristae shape protein Opa1 requires mitochondrial ATP synthase oligomers to reduce ROS accumulation. In cells fueled with galactose to force ATP production by mitochondria, cristae are enlarged, ATP synthase oligomers destabilized, and ROS accumulate.
View Article and Find Full Text PDFTriacylglycerol synthesis enhances macrophage inflammatory function.
Nat Commun
August 2020
Department of Immunometabolism, Max Planck Institute of Epigenetics and Immunobiology, Freiburg im Breisgau, Germany.
Foamy macrophages, which have prominent lipid droplets (LDs), are found in a variety of disease states. Toll-like receptor agonists drive triacylglycerol (TG)-rich LD development in macrophages. Here we explore the basis and significance of this process.
View Article and Find Full Text PDFHost dysbiosis negatively impacts IL-9-producing T-cell differentiation and antitumour immunity.
Br J Cancer
August 2020
Laboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Background: Host-microbiota interactions shape T-cell differentiation and promote tumour immunity. Although IL-9-producing T cells have been described as potent antitumour effectors, their role in microbiota-mediated tumour control remains unclear.
Methods: We analysed the impact of the intestinal microbiota on the differentiation of colonic lamina propria IL-9-producing T cells in germ-free and dysbiotic mice.
Cell-intrinsic metabolic regulation of mononuclear phagocyte activation: Findings from the tip of the iceberg.
Immunol Rev
May 2020
Department of Immunometabolism, Max Planck Institute of Epigenetics and Immunobiology, Freiburg im Breisgau, Germany.
Article Synopsis
- Recent research shows that immune cell activation leads to major changes in metabolism, impacting areas such as gene transcription and protein modifications.
- The focus of this study is on how inflammatory signals (like LPS and IFNγ) versus alternative signals (like IL-4) affect metabolic reprogramming, particularly in dendritic cells and macrophages.
- While there has been significant progress in understanding mononuclear phagocyte metabolism, challenges remain, including the influence of tissue environment on metabolism and how findings in mice correlate to human biology.
Mitochondrial Membrane Potential Regulates Nuclear Gene Expression in Macrophages Exposed to Prostaglandin E2.
Immunity
December 2018
Department of Immunometabolism, Max Planck Institute of Epigenetics and Immunobiology, Freiburg im Breisgau, Germany; Faculty of Biology, University of Freiburg, Freiburg im Breisgau, Germany. Electronic address:
Article Synopsis
- Metabolic engagement is crucial for immune cell function, and prostaglandin E2 (PGE2) impacts macrophage activation and metabolism.
- The study found that PGE2 leads to a loss of mitochondrial membrane potential (Δψ) in interleukin-4-activated macrophages, primarily through changes in gene expression related to the malate-aspartate shuttle.
- This loss of Δψ results in the altered expression of 126 voltage-regulated genes, with a significant role played by the transcription factor ETS variant 1 (ETV1) in regulating a substantial portion of these genes.