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Your search keyword '"Stengel, Stephanie T"' showing total 4 results
Start Over Author "Stengel, Stephanie T" Publisher rockefeller university press
4 results on '"Stengel, Stephanie T"'

1. Intelectin-1 binds and alters the localization of the mucus barrier–modifying bacterium Akkermansia muciniphila

Author

Matute, Juan D., primary, Duan, Jinzhi, additional, Flak, Magdalena B., additional, Griebel, Paul, additional, Tascon-Arcila, Jose A., additional, Doms, Shauni, additional, Hanley, Thomas, additional, Antanaviciute, Agne, additional, Gundrum, Jennifer, additional, Mark Welch, Jessica L., additional, Sit, Brandon, additional, Abtahi, Shabnam, additional, Fuhler, Gwenny M., additional, Grootjans, Joep, additional, Tran, Florian, additional, Stengel, Stephanie T., additional, White, James R., additional, Krupka, Niklas, additional, Haller, Dirk, additional, Clare, Simon, additional, Lawley, Trevor D., additional, Kaser, Arthur, additional, Simmons, Alison, additional, Glickman, Jonathan N., additional, Bry, Lynn, additional, Rosenstiel, Philip, additional, Borisy, Gary, additional, Waldor, Matthew K., additional, Baines, John F., additional, Turner, Jerrold R., additional, and Blumberg, Richard S., additional

Published
2022
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2. ATG16L1 orchestrates interleukin-22 signaling in the intestinal epithelium via cGAS-STING

Author

Aden, Konrad, Tran, Florian, Ito, Go, Sheibani-Tezerji, Raheleh, Lipinski, Simone, Kuiper, Jan W, Tschurtschenthaler, Markus, Saveljeva, Svetlana, Bhattacharyya, Joya, Häsler, Robert, Bartsch, Kareen, Luzius, Anne, Jentzsch, Marlene, Falk-Paulsen, Maren, Stengel, Stephanie T, Welz, Lina, Schwarzer, Robin, Rabe, Björn, Barchet, Winfried, Krautwald, Stefan, Hartmann, Gunther, Pasparakis, Manolis, Blumberg, Richard S, Schreiber, Stefan, Kaser, Arthur, Rosenstiel, Philip, Tran, Florian [0000-0002-3735-9872], Lipinski, Simone [0000-0002-9322-7372], Tschurtschenthaler, Markus [0000-0002-0060-4790], Bhattacharyya, Joya [0000-0003-1745-4167], Krautwald, Stefan [0000-0001-7768-2132], Blumberg, Richard S [0000-0002-9704-248X], Kaser, Arthur [0000-0003-1419-3344], Rosenstiel, Philip [0000-0002-9692-8828], and Apollo - University of Cambridge Repository

Subjects
Mice, Knockout, Interleukins, Autophagy-Related Proteins, Genetic Variation, Membrane Proteins, Inflammatory Bowel Diseases, digestive system, Nucleotidyltransferases, Mice, Animals, Humans, Caco-2 Cells, Intestinal Mucosa, Carrier Proteins, Signal Transduction
Abstract

A coding variant of the inflammatory bowel disease (IBD) risk gene ATG16L1 has been associated with defective autophagy and deregulation of endoplasmic reticulum (ER) function. IL-22 is a barrier protective cytokine by inducing regeneration and antimicrobial responses in the intestinal mucosa. We show that ATG16L1 critically orchestrates IL-22 signaling in the intestinal epithelium. IL-22 stimulation physiologically leads to transient ER stress and subsequent activation of STING-dependent type I interferon (IFN-I) signaling, which is augmented in Atg16l1 ΔIEC intestinal organoids. IFN-I signals amplify epithelial TNF production downstream of IL-22 and contribute to necroptotic cell death. In vivo, IL-22 treatment in Atg16l1 ΔIEC and Atg16l1 ΔIEC/Xbp1 ΔIEC mice potentiates endogenous ileal inflammation and causes widespread necroptotic epithelial cell death. Therapeutic blockade of IFN-I signaling ameliorates IL-22-induced ileal inflammation in Atg16l1 ΔIEC mice. Our data demonstrate an unexpected role of ATG16L1 in coordinating the outcome of IL-22 signaling in the intestinal epithelium.

Published
2018
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3. ATG16L1 orchestrates interleukin-22 signaling in the intestinal epithelium via cGAS–STING

Author

Aden, Konrad, primary, Tran, Florian, additional, Ito, Go, additional, Sheibani-Tezerji, Raheleh, additional, Lipinski, Simone, additional, Kuiper, Jan W., additional, Tschurtschenthaler, Markus, additional, Saveljeva, Svetlana, additional, Bhattacharyya, Joya, additional, Häsler, Robert, additional, Bartsch, Kareen, additional, Luzius, Anne, additional, Jentzsch, Marlene, additional, Falk-Paulsen, Maren, additional, Stengel, Stephanie T., additional, Welz, Lina, additional, Schwarzer, Robin, additional, Rabe, Björn, additional, Barchet, Winfried, additional, Krautwald, Stefan, additional, Hartmann, Gunther, additional, Pasparakis, Manolis, additional, Blumberg, Richard S., additional, Schreiber, Stefan, additional, Kaser, Arthur, additional, and Rosenstiel, Philip, additional

Published
2018
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4. Intelectin-1 binds and alters the localization of the mucus barrier-modifying bacterium Akkermansia muciniphila.

Author

Matute JD, Duan J, Flak MB, Griebel P, Tascon-Arcila JA, Doms S, Hanley T, Antanaviciute A, Gundrum J, Mark Welch JL, Sit B, Abtahi S, Fuhler GM, Grootjans J, Tran F, Stengel ST, White JR, Krupka N, Haller D, Clare S, Lawley TD, Kaser A, Simmons A, Glickman JN, Bry L, Rosenstiel P, Borisy G, Waldor MK, Baines JF, Turner JR, and Blumberg RS

Subjects
Humans, Mice, Animals, Mucus metabolism, Lectins, Verrucomicrobia metabolism, Colitis, Ulcerative metabolism, Colitis, Ulcerative microbiology, Colitis, Ulcerative pathology
Abstract

Intelectin-1 (ITLN1) is a lectin secreted by intestinal epithelial cells (IECs) and upregulated in human ulcerative colitis (UC). We investigated how ITLN1 production is regulated in IECs and the biological effects of ITLN1 at the host-microbiota interface using mouse models. Our data show that ITLN1 upregulation in IECs from UC patients is a consequence of activating the unfolded protein response. Analysis of microbes coated by ITLN1 in vivo revealed a restricted subset of microorganisms, including the mucolytic bacterium Akkermansia muciniphila. Mice overexpressing intestinal ITLN1 exhibited decreased inner colonic mucus layer thickness and closer apposition of A. muciniphila to the epithelial cell surface, similar to alterations reported in UC. The changes in the inner mucus layer were microbiota and A. muciniphila dependent and associated with enhanced sensitivity to chemically induced and T cell-mediated colitis. We conclude that by determining the localization of a select group of bacteria to the mucus layer, ITLN1 modifies this critical barrier. Together, these findings may explain the impact of ITLN1 dysregulation on UC pathogenesis., (© 2022 Matute et al.)

Published
2023
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