Robert D. Thurston
University of Arizona
8 Papers
102 Citations
Robert D. Thurston is an academic researcher from University of Arizona. The author has contributed to research in topics: Colitis & Proinflammatory cytokine. The author has an hindex of 8, co-authored 8 publications.
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Papers
Dendritic cell-specific disruption of TGF-β receptor II leads to altered regulatory T cell phenotype and spontaneous multiorgan autoimmunity
Rajalakshmy Ramalingam,Claire B. Larmonier,Robert D. Thurston,Monica T. Midura-Kiela,Song Guo Zheng,Fayez K. Ghishan,Pawel R. Kiela +6 more
TL;DR: In vivo, in vivo, TGF-β signaling in DCs is critical in the control of autoimmunity through both Treg-dependent and -independent mechanisms, but it does not affect MHCII and costimulatory molecule expression.
Colonic gene expression profile in NHE3-deficient mice: evidence for spontaneous distal colitis.
Daniel Laubitz,Claire B. Larmonier,Aiping Bai,Monica T. Midura-Kiela,Maciej A. Lipko,Robert D. Thurston,Pawel R. Kiela,Fayez K. Ghishan +7 more
TL;DR: It is described that NHE3-deficient mice spontaneously develop colitis restricted to distal colonic mucosa, an observation suggesting a potentially novel role of N HE3 as a modifier gene, which when downregulated during infectious or chronic colitis may modulate the extent and severity of colonic inflammation.
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Limited effects of dietary curcumin on Th-1 driven colitis in IL-10 deficient mice suggest an IL-10-dependent mechanism of protection
Claire B. Larmonier,Jennifer K. Uno,Jennifer K. Uno,Kang Moon Lee,Thomas Karrasch,Daniel Laubitz,Robert D. Thurston,Monica T. Midura-Kiela,Fayez K. Ghishan,Ryan Balfour Sartor,Christian Jobin,Pawel R. Kiela +11 more
TL;DR: In conclusion, curcumin demonstrates limited effectiveness on Th-1 mediated colitis in IL-10(-/-) mice, with moderately improved colonic morphology, but with no significant effect on pathogenic T cell responses and in situ NF-kappaB activity.
79
Changes in mucosal homeostasis predispose NHE3 knockout mice to increased susceptibility to DSS-induced epithelial injury.
Pawel R. Kiela,Daniel Laubitz,Claire B. Larmonier,Monica T. Midura-Kiela,Maciej A. Lipko,Nona Janikashvili,Aiping Bai,Robert D. Thurston,Fayez K. Ghishan +8 more
TL;DR: Results suggest that NHE3 participates in mucosal responses to epithelial damage, acting as a modifier gene determining the extent of the gut inflammatory responses in the face of intestinal injury.
58
NHE3 modulates the severity of colitis in IL-10-deficient mice
Claire B. Larmonier,D. Laubitz,Robert D. Thurston,Alaxis L Bucknam,Faihza M. Hill,Monica T. Midura-Kiela,Rajalakshmy Ramalingam,Pawel R. Kiela,Fayez K. Ghishan +8 more
TL;DR: Chronic NHE3 inhibition or underexpression observed in IBD may contribute to the pathogenesis of IBD by influencing the extent of the epithelial barrier defect and affect the ultimate degree of inflammation.