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  1. Article ; Online: A human milk oligosaccharide prevents intestinal inflammation in adulthood via modulating gut microbial metabolism.

    Schalich, Kasey M / Buendia, Matthew A / Kaur, Harpreet / Choksi, Yash A / Washington, M Kay / Codreanu, Gabriela S / Sherrod, Stacy D / McLean, John A / Peek, Richard M / Acra, Sari A / Townsend, Steven D / Yan, Fang

    mBio

    2024  Volume 15, Issue 4, Page(s) e0029824

    Abstract: Observational evidence suggests that human milk oligosaccharides (HMOs) promote the growth of commensal bacteria in early life and adulthood. However, the mechanisms by which HMOs benefit health through modulation of gut microbial homeostasis remain ... ...

    Abstract Observational evidence suggests that human milk oligosaccharides (HMOs) promote the growth of commensal bacteria in early life and adulthood. However, the mechanisms by which HMOs benefit health through modulation of gut microbial homeostasis remain largely unknown. 2'-fucosyllactose (2'-FL) is the most abundant oligosaccharide in human milk and contributes to the essential health benefits associated with human milk consumption. Here, we investigated how 2'-FL prevents colitis in adulthood through its effects on the gut microbial community. We found that the gut microbiota from adult mice that consumed 2'-FL exhibited an increase in abundance of several health-associated genera, including
    MeSH term(s) Adult ; Humans ; Animals ; Mice ; Milk, Human ; Gastrointestinal Microbiome ; Colitis, Ulcerative/metabolism ; Oligosaccharides/metabolism ; Colitis/prevention & control ; Inflammation ; Pantothenic Acid/analogs & derivatives
    Chemical Substances dexpanthenol (1O6C93RI7Z) ; Oligosaccharides ; Pantothenic Acid (19F5HK2737)
    Language English
    Publishing date 2024-03-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2557172-2
    ISSN 2150-7511 ; 2161-2129
    ISSN (online) 2150-7511
    ISSN 2161-2129
    DOI 10.1128/mbio.00298-24
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Accumulation of long-chain fatty acids in the tumor microenvironment drives dysfunction in intrapancreatic CD8+ T cells.

    Manzo, Teresa / Prentice, Boone M / Anderson, Kristin G / Raman, Ayush / Schalck, Aislyn / Codreanu, Gabriela S / Nava Lauson, Carina B / Tiberti, Silvia / Raimondi, Andrea / Jones, Marissa A / Reyzer, Michelle / Bates, Breanna M / Spraggins, Jeffrey M / Patterson, Nathan H / McLean, John A / Rai, Kunal / Tacchetti, Carlo / Tucci, Sara / Wargo, Jennifer A /
    Rodighiero, Simona / Clise-Dwyer, Karen / Sherrod, Stacy D / Kim, Michael / Navin, Nicholas E / Caprioli, Richard M / Greenberg, Philip D / Draetta, Giulio / Nezi, Luigi

    The Journal of experimental medicine

    2020  Volume 217, Issue 8

    Abstract: CD8+ T cells are master effectors of antitumor immunity, and their presence at tumor sites correlates with favorable outcomes. However, metabolic constraints imposed by the tumor microenvironment (TME) can dampen their ability to control tumor ... ...

    Abstract CD8+ T cells are master effectors of antitumor immunity, and their presence at tumor sites correlates with favorable outcomes. However, metabolic constraints imposed by the tumor microenvironment (TME) can dampen their ability to control tumor progression. We describe lipid accumulation in the TME areas of pancreatic ductal adenocarcinoma (PDA) populated by CD8+ T cells infiltrating both murine and human tumors. In this lipid-rich but otherwise nutrient-poor TME, access to using lipid metabolism becomes particularly valuable for sustaining cell functions. Here, we found that intrapancreatic CD8+ T cells progressively accumulate specific long-chain fatty acids (LCFAs), which, rather than provide a fuel source, impair their mitochondrial function and trigger major transcriptional reprogramming of pathways involved in lipid metabolism, with the subsequent reduction of fatty acid catabolism. In particular, intrapancreatic CD8+ T cells specifically exhibit down-regulation of the very-long-chain acyl-CoA dehydrogenase (VLCAD) enzyme, which exacerbates accumulation of LCFAs and very-long-chain fatty acids (VLCFAs) that mediate lipotoxicity. Metabolic reprogramming of tumor-specific T cells through enforced expression of ACADVL enabled enhanced intratumoral T cell survival and persistence in an engineered mouse model of PDA, overcoming one of the major hurdles to immunotherapy for PDA.
    MeSH term(s) Acyl-CoA Dehydrogenase, Long-Chain/biosynthesis ; Acyl-CoA Dehydrogenase, Long-Chain/genetics ; Animals ; CD8-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/pathology ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/metabolism ; Carcinoma, Pancreatic Ductal/pathology ; Down-Regulation ; Fatty Acids/genetics ; Fatty Acids/metabolism ; Gene Expression Regulation, Enzymologic ; Gene Expression Regulation, Neoplastic ; Lymphocytes, Tumor-Infiltrating/metabolism ; Lymphocytes, Tumor-Infiltrating/pathology ; Mice ; Mice, Mutant Strains ; Neoplasm Proteins/biosynthesis ; Neoplasm Proteins/genetics ; Pancreas/metabolism ; Pancreas/pathology ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; Tumor Microenvironment
    Chemical Substances Fatty Acids ; Neoplasm Proteins ; Acyl-CoA Dehydrogenase, Long-Chain (EC 1.3.8.8)
    Language English
    Publishing date 2020-06-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 218343-2
    ISSN 1540-9538 ; 0022-1007
    ISSN (online) 1540-9538
    ISSN 0022-1007
    DOI 10.1084/jem.20191920
    Database MEDical Literature Analysis and Retrieval System OnLINE

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