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4. An essential role of adenosine deaminase acting on RNA 1 in coeliac disease mucosa

Author

Di Fusco, D, Segreto, Mt, Iannucci, A, Maresca, C, Franzè, E, Di Maggio, G, Di Grazia, A, Boccanera, S, Laudisi, F, Marafini, I, Paoluzi, Oa, Michenzi, A, Monteleone, G, and Monteleone, I

Subjects
Immunology, Immunology and Allergy, dsRNA, virus, Settore MED/50, IFN, ADAR, celiac disease
Abstract

Background and aimType I interferons (IFNs) are highly expressed in the gut mucosa of celiac disease (CD) gut mucosa and stimulates immune response prompted by gluten ingestion, but the processes that maintain the production of these inflammatory molecules are not well understood. Adenosine deaminase acting on RNA 1 (ADAR1), an RNA-editing enzyme, plays a crucial role in inhibiting self or viral RNAs from activating auto-immune mediated responses, most notably within the type-I IFN production pathway. The aim of this study was to assess whether ADAR1 could contribute to the induction and/or progression of gut inflammation in patients with celiac disease.Material and methodsADAR1 expression was assessed by Real time PCR and Western blotting in duodenal biopsy taken from inactive and active celiac disease (CD) patients and normal controls (CTR). To analyze the role of ADAR1 in inflamed CD mucosa, lamina propria mononuclear cells (LPMC) were isolated from inactive CD and ADAR1 was silenced in with a specific antisense oligonucleotide (AS) and then incubated with a synthetic analogue of viral dsRNA (poly I:C). IFN-inducing pathways (IRF3, IRF7) in these cells were evaluated with Western blotting and inflammatory cytokines were evaluated with flow cytometry. Lastly, the role of ADAR1 was investigated in a mouse model of poly I:C-driven small intestine atrophy.ResultsReduced ADAR1 expression was seen in duodenal biopsies compared to inactive CD and normal controls. Ex vivo organ cultures of duodenal mucosal biopsies, taken from inactive CD patients, stimulated with a peptic-tryptic digest of gliadin displayed a decreased expression of ADAR1. ADAR1 silencing in LPMC stimulated with a synthetic analogue of viral dsRNA strongly boosted the activation of IRF3 and IRF7 and the production of type-I IFN, TNF-α and IFN-γ. Administration of ADAR1 antisense but not sense oligonucleotide to mice with poly I:C-induced intestinal atrophy, significantly increased gut damage and inflammatory cytokines production.ConclusionsThese data show that ADAR1 is an important regulator of intestinal immune homeostasis and demonstrate that defective ADAR1 expression could provide to amplifying pathogenic responses in CD intestinal mucosa.

Published
2023
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5. T.07.3 HEPCIDIN SUSTAINS COLORECTAL CANCER CELL SURVIVAL

Author

Di Grazia, A., primary, Di Fusco, D., additional, Laudisi, F., additional, Di Maggio, G., additional, Franzè, E., additional, Maresca, C., additional, Segreto, M.T., additional, Sica, G., additional, Stolfi, C., additional, Monteleone, I., additional, and Monteleone, G., additional

Published
2022
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7. Tbet Expression in Regulatory T Cells Is Required to Initiate Th1-Mediated Colitis

Author

Di Giovangiulio, M, Rizzo, A, Franzè, E, Caprioli, F, Facciotti, F, Onali, S, Favale, A, Stolfi, C, Fehling, H, Monteleone, G, Fantini, M, Di Giovangiulio M, Rizzo A, Franzè E, Caprioli F, Facciotti F, Onali S, Favale A, Stolfi C, Fehling HJ, Monteleone G, Fantini MC, Di Giovangiulio, M, Rizzo, A, Franzè, E, Caprioli, F, Facciotti, F, Onali, S, Favale, A, Stolfi, C, Fehling, H, Monteleone, G, Fantini, M, Di Giovangiulio M, Rizzo A, Franzè E, Caprioli F, Facciotti F, Onali S, Favale A, Stolfi C, Fehling HJ, Monteleone G, and Fantini MC

Abstract

In normal conditions gut homeostasis is maintained by the suppressive activity of regulatory T cells (Tregs), characterized by the expression of the transcription factor FoxP3. In human inflammatory bowel disease, which is believed to be the consequence of the loss of tolerance toward antigens normally contained in the gut lumen, Tregs have been found to be increased and functionally active, thus pointing against their possible role in the pathogenesis of this immune-mediated disease. Though, in inflammatory conditions, Tregs have been shown to upregulate the T helper (Th) type 1-related transcription factor Tbet and to express the pro-inflammatory cytokine IFN gamma, thus suggesting that at a certain point of the inflammatory process, Tregs might contribute to inflammation rather than suppress it. Starting from the observation that Tregs isolated from the lamina propria of active but not inactive IBD patients or uninflamed controls express Tbet and IFN gamma, we investigated the functional role of Th1-like Tregs in the dextran sulfate model of colitis. As observed in human IBD, Th1-like Tregs were upregulated in the inflamed lamina propria of treated mice and the expression of Tbet and IFN gamma in Tregs preceded the accumulation of conventional Th1 cells. By using a Treg-specific Tbet conditional knockout, we demonstrated that Tbet expression in Tregs is required for the development of colitis. Indeed, Tbet knockout mice developed milder colitis and showed an impaired Th1 immune response. In these mice not only the Tbet deficient Tregs but also the Tbet proficient conventional T cells showed reduced IFN gamma expression. However, Tbet deficiency did not affect the Tregs suppressive capacity in vitro and in vivo in the adoptive transfer model of colitis. In conclusion here we show that Tbet expression by Tregs sustains the early phase of the Th1-mediated inflammatory response in the gut.

Published
2019

9. OC.06.5 GATA6 DEFICIENCY LEADS TO EPITHELIAL BARRIER DYSFUNCTION AND ENHANCES SUSCEPTIBILITY TO GUT INFLAMMATION

Author

Laudisi, F., primary, Stolfi, C., additional, Bevivino, G., additional, Maresca, C., additional, Franzè, E., additional, Troncone, E., additional, Lolli, E., additional, Marafini, I., additional, Pietrucci, D., additional, Teofani, A., additional, Di Grazia, A., additional, Di Fusco, D., additional, Colantoni, A., additional, Ortenzi, A., additional, Desideri, A., additional, Monteleone, I., additional, and Monteleone, G., additional

Published
2021
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11. Follistatin-like protein 1 sustains colon cancer cell growth and survival

Author

Bevivino, G, Sedda, S, Franzè, E, Stolfi, C, Di Grazia, A, Dinallo, V, Caprioli, F, Facciotti, F, Colantoni, A, Ortenzi, A, Rossi, P, Monteleone, G, Bevivino G, Sedda S, Franzè E, Stolfi C, Di Grazia A, Dinallo V, Caprioli F, Facciotti F, Colantoni A, Ortenzi A, Rossi P, Monteleone G, Bevivino, G, Sedda, S, Franzè, E, Stolfi, C, Di Grazia, A, Dinallo, V, Caprioli, F, Facciotti, F, Colantoni, A, Ortenzi, A, Rossi, P, Monteleone, G, Bevivino G, Sedda S, Franzè E, Stolfi C, Di Grazia A, Dinallo V, Caprioli F, Facciotti F, Colantoni A, Ortenzi A, Rossi P, and Monteleone G

Abstract

Follistatin-like protein 1 (FSTL1) is a secreted glycoprotein, which controls several physiological and pathological events. FSTL1 expression is deregulated in many tumors, but its contribution to colon carcinogenesis is not fully understood. Here, we investigated the expression and functional role of FSTL1 in colorectal cancer (CRC). A significant increase of FSTL1 was seen in human CRC as compared to the surrounding non-tumor tissues and this occurred at both RNA and protein level. Knockdown of FSTL1 in CRC cells with a specific antisense oligonucleotide (AS) reduced expression of regulators of the late G1 phase, such as phosphorylated retinoblastoma protein, E2F-1, cyclin E and phospho-cyclin-dependent kinase-2, and promoted accumulation of cells in the G1 phase of the cell cycle thus resulting in diminished cell proliferation. Consistently, recombinant FSTL1 induced proliferation of normal intestinal epithelial cells through an ERK1/2-dependent mechanism. Cell cycle arrest driven by FSTL1 AS in CRC cells was accompanied by activation of caspases and subsequent induction of apoptosis. Moreover, FSTL1 knockdown made CRC cells more susceptible to oxaliplatin and irinotecan-induced death. Data indicate that FSTL1 is over-expressed in human CRC and suggest a role for this protein in favouring intestinal tumorigenesis.

Published
2018

12. OC.16.3 THE FRAGILE X MENTAL RETARDATION PROTEIN REGULATES RIP1K AND COLORECTAL CANCER RESISTANCE TO NECROPTOSIS

Author

Di Grazia, A., primary, Marafini, I., additional, Pedini, G., additional, Di Fusco, D., additional, Laudisi, F., additional, Dinallo, V., additional, Pacini, L., additional, Stolfi, C., additional, Franzè, E., additional, Sileri, P., additional, Sica, G., additional, Monteleone, G., additional, Bagni, C., additional, and Monteleone, I., additional

Published
2020
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19. OC.10.1 RECIPROCAL REGULATION BETWEEN SMAD7 AND SIRT1 IN THE GUT

Author

Sedda, S., primary, Franzè, E., additional, Di Giovangiulio, M., additional, Rizzo, A., additional, Bevivino, G., additional, Colantoni, A., additional, Ortenzi, A., additional, Sileri, P., additional, Sica, G.S., additional, Fantini, M.C., additional, and Monteleone, G., additional

Published
2018
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25. Defective expression of SIRT1 contributes to sustain inflammatory pathways in the gut

Author

Caruso, R, primary, Marafini, I, additional, Franzè, E, additional, Stolfi, C, additional, Zorzi, F, additional, Monteleone, I, additional, Caprioli, F, additional, Colantoni, A, additional, Sarra, M, additional, Sedda, S, additional, Biancone, L, additional, Sileri, P, additional, Sica, G S, additional, MacDonald, T T, additional, Pallone, F, additional, and Monteleone, G, additional

Published
2014
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39. IL-15 positively regulates IL-21 production in celiac disease mucosa

Author

Sarra, M, primary, Cupi, M L, additional, Monteleone, I, additional, Franzè, E, additional, Ronchetti, G, additional, Di Sabatino, A, additional, Gentileschi, P, additional, Franceschilli, L, additional, Sileri, P, additional, Sica, G, additional, Del Vecchio Blanco, G, additional, Cretella, M, additional, Paoluzi, O A, additional, Corazza, G R, additional, Pallone, F, additional, and Monteleone, G, additional

Published
2013
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40. P.05.11 HIGH EXPRESSION OF THE “A DISINTEGRIN AND METALLOPROTEASE” 19 (ADAM19), A SHEDDASE FOR TNF-α IN THE MUCOSA OF PATIENTS WITH INFLAMMATORY BOWEL DISEASES

Author

Franzè, E., primary, Caruso, R., additional, Stolfi, C., additional, Sarra, M., additional, Cupi, M.L., additional, Caprioli, F., additional, Ronchetti, G., additional, Salvatori, I., additional, Sedda, S., additional, Ascolani, M., additional, Antenucci, C., additional, Biancone, L., additional, Pallone, F., additional, and Monteleone, G., additional

Published
2012
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41. OC.08.6 2-METHOXY-5-AMINO-N-HYDROXYBENZAMIDE, A DERIVATIVE OF MESALAMINE, INHIBITS COLON CANCER CELL GROWTH THROUGH CYCLOOXYGENASE-2-DEPENDENT AND -INDEPENDENT MECHANISMS

Author

Stolfi, C., primary, Franzè, E., additional, Monteleone, I., additional, Caruso, R., additional, Franceschilli, L., additional, Sileri, P., additional, Sica, G., additional, Gaspari, A.L., additional, Del Vecchio Blanco, G., additional, Pallone, F., additional, and Monteleone, G., additional

Published
2012
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