Articles by Daniele Corridoni in JoVE
Flexible Colonoscopy in Mice to Evaluate the Severity of Colitis and Colorectal Tumors Using a Validated Endoscopic Scoring System Tomohiro Kodani*1,3, Alex Rodriguez-Palacios*1,3, Daniele Corridoni1,3, Loris Lopetuso2,3, Luca Di Martino1,3, Brian Marks1,3, James Pizarro1,3, Theresa Pizarro2,3, Amitabh Chak1,3, Fabio Cominelli1,3 1Division of Gastroenterology, Case Western Reserve University School of Medicine, Cleveland, 2Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, 3Digestive Health Research Center, Case Western Reserve University School of Medicine, Cleveland Over the past few years, new generation endoscopes have emerged as important diagnostic research aids for evaluating murine colitis and colorectal tumors. We present herein a detailed protocol for endoscopic assessment of inflammation and colorectal tumors in mice, as well as a novel scoring system that uses decimal identifiers to document the endoscopic severity of colitis and colorectal tumors.
Other articles by Daniele Corridoni on PubMed
New Insights into the Dichotomous Role of Innate Cytokines in Gut Homeostasis and Inflammation Cytokine. Sep, 2012 | Pubmed ID: 22795953 In addition to their well-known role in acute injury and chronic inflammation, "innate" cytokines play an important role in health and the maintenance of normal immune homeostasis. This group includes the prototypic cytokines IL-1 and TNFÎ±, as well as several other members belonging to the IL-1 and TNF family, such as IL-18, IL-33, IL-36-38, and TL1A. The dichotomous role of these cytokines has been best characterized in the intestine where innate cytokines may play both a protective and a pro-inflammatory role, depending upon the immmunological status of the host or the type and phase of the inflammatory process. This new information has produced novel pathogenetic hypotheses that have important translational implications both in regard to the prevention and treatment of chronic intestinal inflammation, including Crohn's disease and ulcerative colitis, the two major forms of inflammatory bowel disease. This review will discuss and summarize current data regarding the role of IL-1, TNFÎ±, and their family members in regulating gut mucosal homeostasis and chronic intestinal inflammation.
Probiotic Bacteria Regulate Intestinal Epithelial Permeability in Experimental Ileitis by a TNF-dependent Mechanism PloS One. 2012 | Pubmed ID: 22848704 We previously showed that the probiotic mixture, VSL#3, prevents the onset of ileitis in SAMP/YitFc (SAMP) mice, and this effect was associated with stimulation of epithelial-derived TNF. The aim of this study was to determine the mechanism(s) of VSL#3-mediated protection on epithelial barrier function and to further investigate the "paradoxical" effects of TNF in preventing SAMP ileitis.
Dysregulated NOD2 Predisposes SAMP1/YitFc Mice to Chronic Intestinal Inflammation Proceedings of the National Academy of Sciences of the United States of America. Sep, 2013 | Pubmed ID: 24082103 Nucleotide-binding oligomerization domain-containing 2 (NOD2) is an intracellular receptor that plays an essential role in innate immunity as a sensor of a component of the bacterial cell wall, muramyl dipeptide (MDP). Crohn's disease (CD)-associated NOD2 variants lead to defective innate immune responses, including decreased NF-ÎºB activation and cytokine production. We report herein that SAMP1/YitFc (SAMP) mice, which develop spontaneous CD-like ileitis in the absence of NOD2 genetic mutations, fail to respond to MDP administration by displaying decreased innate cytokine production and dysregulated NOD2 signaling compared with parental AKR control mice. We show that, unlike in other mouse strains, in vivo administration of MDP does not prevent dextran sodium sulfate-induced colitis in SAMP mice and that the abnormal NOD2 response is specific to the hematopoietic cellular component. Moreover, we demonstrate that MDP fails to enhance intracellular bacterial killing in SAMP mice. These findings shed important light on the initiating molecular events underlying CD-like ileitis.