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3. Lymphocytic colitis can be transcriptionally divided into channelopathic and inflammatory lymphocytic colitis

Author

Bhardwaj, Archana, Münch, Andreas, Montague, Julia, Koch, Stefan, Rosenstiel, Philip, Escudero-Hernández, Celia, Bhardwaj, Archana, Münch, Andreas, Montague, Julia, Koch, Stefan, Rosenstiel, Philip, and Escudero-Hernández, Celia

Abstract

BackgroundThe pathobiology of the non-destructive inflammatory bowel disease (IBD) lymphocytic colitis (LC) is poorly understood. We aimed to define an LC-specific mucosal transcriptome to gain insight into LC pathology, identify unique genomic signatures, and uncover potentially druggable disease pathways.MethodsWe performed bulk RNA-sequencing of LC and collagenous colitis (CC) colonic mucosa from patients with active disease, and healthy controls (n = 4-10 per cohort). Differential gene expression was analyzed by gene-set enrichment and deconvolution analyses to identify pathologically relevant pathways and cells, respectively, altered in LC. Key findings were validated using reverse transcription quantitative PCR and/or immunohistochemistry. Finally, we compared our data with a previous cohort of ulcerative colitis and Crohn's disease patients (n = 4 per group) to distinguish non-destructive from classic IBD.ResultsLC can be subdivided into channelopathic LC, which is governed by organic acid and ion transport dysregulation, and inflammatory LC, which is driven by microbial immune responses. Inflammatory LC displays an innate and adaptive immunity that is limited compared to CC and classic IBD. Conversely, we noted a distinct induction of regulatory non-coding RNA species in inflammatory LC samples. Moreover, compared with CC, water channel and cell adhesion molecule gene expression decreased in channelopathic LC, whereas it was accentuated in inflammatory LC and associated with reduced intestinal epithelial cell proliferation.ConclusionsWe conclude that LC can be subdivided into channelopathic LC and inflammatory LC that could be pathomechanistically distinct subtypes despite their shared clinical presentation. Inflammatory LC exhibits a dampened immune response compared to CC and classic IBDs. Our results point to regulatory micro-RNAs as a potential disease-specific feature that may be amenable to therapeutic intervention. image, Funding Agencies|Knut och Alice Wallenbergs Stiftelse; Deutsche Forschungsgemeinschaft; Ferring; Region Ostergotland

Published
2024
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13. Up-regulation of gasdermin C in mouse small intestine is associated with lytic cell death in enterocytes in worm-induced type 2 immunity.

Author

Ranhui Xi, Montague, Julia, Xiaoli Lin, Chanyi Lu, Weiwei Lei, Keisuke Tanaka, Zhang, Yali V., Xin Xu, Xin Zheng, Xuedong Zhou, Urban Jr, Joseph F., Ken Iwatsuki, Margolskee, Robert F., Matsumoto, Ichiro, Tizzano, Marco, Jiyao Li, and Peihua Jiang

Subjects
*CELL death, *ENTEROCYTES, *SMALL intestine, *LABORATORY mice, *INNATE lymphoid cells, *COMMERCIAL products, *CURCUMIN
Abstract

"Taste-like" tuft cells in the intestine trigger type 2 immunity in response toworm infection. The secretion of interleukin-13 (IL-13) from type 2 innate lymphoid cells (ILC2) represents a key step in the tuft cell-ILC2 cell-intestinal epithelial cell circuit that drives the clearance of worms from the gut via type 2 immune responses. Hallmark features of type 2 responses include tissue remodeling, such as tuft and goblet cell expansion, and villus atrophy, yet it remains unclear if additional molecular changes in the gut epithelium facilitate the clearance of worms from the gut. Using gut organoids, we demonstrated that IL-4 and IL-13, two type 2 cytokines with similar functions, not only induced the classical type 2 responses (e.g., tuft cell expansion) but also drastically up-regulated the expression of gasdermin C genes (Gsdmcs). Using an in vivo worm-induced type 2 immunity model, we confirmed the up-regulation of Gsdmcs in Nippostrongylus brasiliensis-infected wild-type C57BL/6 mice. Consistent with gasdermin family members being principal effectors of pyroptosis, overexpression of Gsdmc2 in human embryonic kidney 293 (HEK293) cells triggered pyroptosis and lytic cell death. Moreover, in intestinal organoids treated with IL-4 or IL-13, or in wild-type mice infected with N. brasiliensis, lytic cell death increased, which may account for villus atrophy observed in worm-infected mice. Thus, we propose that the up-regulated Gsdmc family may be major effectors for type 2 responses in the gut and that Gsdmc-mediated pyroptosis may provide a conduit for the release of antiparasitic factors from enterocytes to facilitate the clearance of worms. [ABSTRACT FROM AUTHOR]

Published
2021
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14. Reply

Author

Ranasinghe, Isuru, Parzynski, Craig S., Searfoss, Rana, Montague, Julia, Lin, Zhenqiu, Allen, John, Vender, Ronald, Bhat, Kanchana, Ross, Joseph S., Bernheim, Susannah, Krumholz, Harlan M., and Drye, Elizabeth

Published
2016
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15. ACUTE ADMISSION RATES FOR PATIENTS WITH HEART FAILURE CARED FOR BY ACCOUNTABLE CARE ORGANIZATIONS

Author

Spatz, Erica, primary, Lipska, Kasia, additional, Dai, Ying, additional, Altaf, Faseeha, additional, Joyce, Erin, additional, Montague, Julia, additional, Bao, Haikun, additional, Sutton, La’Mont, additional, Parzynski, Craig, additional, Herrin, Jeph, additional, Zhang, Vera, additional, Ross, Joseph, additional, Lin, Zhenqiu, additional, Bernheim, Susannah, additional, Krumholz, Harlan, additional, and Drye, Elizabeth, additional

Published
2015
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