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Crohn Disease: HELP
Articles by Sergio Rutella
Based on 3 articles published since 2008

Between 2008 and 2019, Sergio Rutella wrote the following 3 articles about Crohn Disease.
+ Citations + Abstracts
1 Editorial Regulatory T-cell therapy for Crohn's disease: in vivo veritas. 2012

Danese, Silvio / Fiorino, Gionata / Rutella, Sergio. ·IBD Center, Gastroenterology, Humanitas Clinical and Research Center, Milan, Italy. Electronic address: sdanese@hotmail.com. · IBD Center, Gastroenterology, Humanitas Clinical and Research Center, Milan, Italy. · Pediatric Hematology/Oncology and Transfusion Medicine, IRCCS Bambino Gesù Children's Hospital, Rome, Italy. ·Gastroenterology · Pubmed #23000230.

ABSTRACT: -- No abstract --

2 Article FOXP3⁺ T regulatory cell modifications in inflammatory bowel disease patients treated with anti-TNFα agents. 2013

Guidi, Luisa / Felice, Carla / Procoli, Annabella / Bonanno, Giuseppina / Martinelli, Enrica / Marzo, Manuela / Mocci, Giammarco / Pugliese, Daniela / Andrisani, Gianluca / Danese, Silvio / De Vitis, Italo / Papa, Alfredo / Armuzzi, Alessandro / Rutella, Sergio. ·Department of Internal Medicine, Inflammatory Bowel Disease Unit, Complesso Integrato Columbus, Catholic University, Largo Gemelli 8, 00168 Rome, Italy. ·Biomed Res Int · Pubmed #24063002.

ABSTRACT: Treg modulation has been hypothesized as one of the mechanisms by which antitumor necrosis factor α (TNFα) agents exert their action in rheumatoid arthritis (RA) and inflammatory bowel disease (IBD). However, data in IBD are still conflicting. We evaluated CD4⁺CD25⁺FOXP3⁺ (Tregs) by flow cytometry in peripheral blood from 32 adult IBD patient before (T0) and after the induction of anti-TNFα therapy (T1). Eight healthy controls (HCs) were included. We also evaluated the number of FOXP3⁺ cells in the lamina propria (LP) in biopsies taken in a subset of patients and controls. Treg frequencies were significantly increased in peripheral blood from our patients after anti-TNFα therapy compared to T0. T1 but not T0 levels were higher than HC. The increase was detectable only in clinical responders to the treatment. A negative correlation was found among delta Treg levels and the age of patients or disease duration and with the activity score of Crohn's disease (CD). No significant differences were found in LP FOXP3⁺ cells. Our data suggest the possibility that in IBD patients the treatment with anti-TNFα may affect Treg percentages and that Treg modifications may correlate with clinical response, but differently in early versus late disease.

3 Article Infliximab therapy inhibits inflammation-induced angiogenesis in the mucosa of patients with Crohn's disease. 2011

Rutella, Sergio / Fiorino, Gionata / Vetrano, Stefania / Correale, Carmen / Spinelli, Antonino / Pagano, Nico / Arena, Vincenzo / Maggiano, Nicola / Repici, Alessandro / Malesci, Alberto / Danese, Silvio. ·Department of Hematology, Catholic University Medical School, Rome, Italy. srutella@rm.unicatt.it ·Am J Gastroenterol · Pubmed #21364546.

ABSTRACT: OBJECTIVES: Inflammation-driven angiogenesis contributes to the pathogenesis of inflammatory bowel disease (IBD). In line with this, the efficacy of inhibitors of angiogenesis has been demonstrated in experimental models of colitis. Currently, the ability of infliximab, an anti-tumor necrosis factor-α (TNF-α) agent that is highly beneficial in patients with IBD, to affect mucosal angiogenesis in patients with Crohn's disease (CD) and ulcerative colitis (UC) is unknown. METHODS: Patients with active CD (n=14) were treated with infliximab for 1 year, and peripheral blood and intestinal mucosa samples were collected before and after treatment. Mucosal angiogenesis was evaluated by CD31 and Ki-67 staining in endoscopic biopsies at baseline (week 0) and at week 54. The release of vascular endothelial growth factor-A (VEGF-A) by cultured mucosal extracts was measured by enzyme-linked immunosorbent assay (ELISA), before and after administration of infliximab, as well as in cultures of human intestinal fibroblasts (HIFs) stimulated with TNF-α in the presence or absence of infliximab. Migration of human intestinal microvascular endothelial cells (HIMECs) was investigated by migration assays. RESULTS: Microvessel density was significantly higher in the mucosa from patients with CD compared with tissue from healthy control individuals. Of the 14 patients, 8 (57%) showed a clinical remission in response to infliximab, which was associated with a significant reduction of microvascular density. Morphometric vessel analysis further confirmed the significant reduction of the area of vascular section after administration of infliximab. Furthermore, the expression levels of the proliferation marker Ki-67 in endothelial cells were significantly reduced after treatment. The mucosal concentration of VEGF-A was also significantly decreased, whereas in vitro exposure of HIF to infliximab virtually abolished TNF-α-induced VEGF-A production. These phenomena did not occur in patients who showed no clinical response to infliximab. CONCLUSIONS: Administration of infliximab downregulates mucosal angiogenesis in patients with CD and restrains production of VEGF-A by mucosal fibroblasts. It is proposed that this ameliorates inflammation-driven angiogenesis in the gut mucosa and contributes to the therapeutic efficacy of blockade of TNF-α.