Adiponectin and plant-derived mammalian adiponectin homolog exert a protective effect in murine colitis

Handle URI:
http://hdl.handle.net/10754/561751
Title:
Adiponectin and plant-derived mammalian adiponectin homolog exert a protective effect in murine colitis
Authors:
Arsenescu, Violeta; Narasimhan, Meena L.; Halide, Tuna; Bressan, Ray Anthony; Barisione, Chiara; Cohen, Donald A.; De Villiers, Willem Js S; Arsenescu, Razvan I.
Abstract:
Background: Hypoadiponectinemia has been associated with states of chronic inflammation in humans. Mesenteric fat hypertrophy and low adiponectin have been described in patients with Crohn's disease. We investigated whether adiponectin and the plant-derived homolog, osmotin, are beneficial in a murine model of colitis. Methods: C57BL/6 mice were injected (i.v.) with an adenoviral construct encoding the full-length murine adiponectin gene (AN+DSS) or a reporter-LacZ (Ctr and V+DSS groups) prior to DSS colitis protocol. In another experiment, mice with DSS colitis received either osmotin (Osm+DSS) or saline (DSS) via osmotic pumps. Disease progression and severity were evaluated using body weight, stool consistency, rectal bleeding, colon lengths, and histology. In vitro experiments were carried out in bone marrow-derived dendritic cells. Results: Mice overexpressing adiponectin had lower expression of proinflammatory cytokines (TNF, IL-1β), adipokines (angiotensin, osteopontin), and cellular stress and apoptosis markers. These mice had higher levels of IL-10, alternative macrophage marker, arginase 1, and leukoprotease inhibitor. The plant adiponectin homolog osmotin similarly improved colitis outcome and induced robust IL-10 secretion. LPS induced a state of adiponectin resistance in dendritic cells that was reversed by treatment with PPARγ agonist and retinoic acid. Conclusion: Adiponectin exerted protective effects during murine DSS colitis. It had a broad activity that encompassed cytokines, chemotactic factors as well as processes that assure cell viability during stressful conditions. Reducing adiponectin resistance or using plant-derived adiponectin homologs may become therapeutic options in inflammatory bowel disease. © 2011 Springer Science+Business Media, LLC.
KAUST Department:
Center for Desert Agriculture; Biological and Environmental Sciences and Engineering (BESE) Division
Publisher:
Springer Science + Business Media
Journal:
Digestive Diseases and Sciences
Issue Date:
11-Apr-2011
DOI:
10.1007/s10620-011-1692-0
PubMed ID:
21479819
Type:
Article
ISSN:
01632116
Sponsors:
This work was supported by grants from Broad Medical Foundation, UCB Inc., Kentucky Science & Engineering Foundation (RA), and from NIH-DK07778-07 (VA). There are no competing financial interests to declare.
Appears in Collections:
Articles; Center for Desert Agriculture; Biological and Environmental Sciences and Engineering (BESE) Division

Full metadata record

DC FieldValue Language
dc.contributor.authorArsenescu, Violetaen
dc.contributor.authorNarasimhan, Meena L.en
dc.contributor.authorHalide, Tunaen
dc.contributor.authorBressan, Ray Anthonyen
dc.contributor.authorBarisione, Chiaraen
dc.contributor.authorCohen, Donald A.en
dc.contributor.authorDe Villiers, Willem Js Sen
dc.contributor.authorArsenescu, Razvan I.en
dc.date.accessioned2015-08-03T09:03:47Zen
dc.date.available2015-08-03T09:03:47Zen
dc.date.issued2011-04-11en
dc.identifier.issn01632116en
dc.identifier.pmid21479819en
dc.identifier.doi10.1007/s10620-011-1692-0en
dc.identifier.urihttp://hdl.handle.net/10754/561751en
dc.description.abstractBackground: Hypoadiponectinemia has been associated with states of chronic inflammation in humans. Mesenteric fat hypertrophy and low adiponectin have been described in patients with Crohn's disease. We investigated whether adiponectin and the plant-derived homolog, osmotin, are beneficial in a murine model of colitis. Methods: C57BL/6 mice were injected (i.v.) with an adenoviral construct encoding the full-length murine adiponectin gene (AN+DSS) or a reporter-LacZ (Ctr and V+DSS groups) prior to DSS colitis protocol. In another experiment, mice with DSS colitis received either osmotin (Osm+DSS) or saline (DSS) via osmotic pumps. Disease progression and severity were evaluated using body weight, stool consistency, rectal bleeding, colon lengths, and histology. In vitro experiments were carried out in bone marrow-derived dendritic cells. Results: Mice overexpressing adiponectin had lower expression of proinflammatory cytokines (TNF, IL-1β), adipokines (angiotensin, osteopontin), and cellular stress and apoptosis markers. These mice had higher levels of IL-10, alternative macrophage marker, arginase 1, and leukoprotease inhibitor. The plant adiponectin homolog osmotin similarly improved colitis outcome and induced robust IL-10 secretion. LPS induced a state of adiponectin resistance in dendritic cells that was reversed by treatment with PPARγ agonist and retinoic acid. Conclusion: Adiponectin exerted protective effects during murine DSS colitis. It had a broad activity that encompassed cytokines, chemotactic factors as well as processes that assure cell viability during stressful conditions. Reducing adiponectin resistance or using plant-derived adiponectin homologs may become therapeutic options in inflammatory bowel disease. © 2011 Springer Science+Business Media, LLC.en
dc.description.sponsorshipThis work was supported by grants from Broad Medical Foundation, UCB Inc., Kentucky Science & Engineering Foundation (RA), and from NIH-DK07778-07 (VA). There are no competing financial interests to declare.en
dc.publisherSpringer Science + Business Mediaen
dc.subjectAdiponectinen
dc.subjectDendritic cellsen
dc.subjectInflammatory bowel diseaseen
dc.subjectMammalian adiponectin homologen
dc.subjectPPARγ agonistsen
dc.titleAdiponectin and plant-derived mammalian adiponectin homolog exert a protective effect in murine colitisen
dc.typeArticleen
dc.contributor.departmentCenter for Desert Agricultureen
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Divisionen
dc.identifier.journalDigestive Diseases and Sciencesen
dc.contributor.institutionDivision of Digestive Diseases and Nutrition, Microbiology, Immunology and Molecular Genetics, University of Kentucky, Medical Center, 800 Rose Street, Lexington, KY 40536, United Statesen
dc.contributor.institutionGraduate Center for Nutritional Sciences, University of Kentucky, Lexington, KY 40536, United Statesen
dc.contributor.institutionMicrobiology, Immunology and Molecular Genetics, University of Kentucky, Lexington, KY 40536, United Statesen
dc.contributor.institutionResearch Center of Cardiovascular Biology, University of Genoa, Liguria 16126, Italyen
dc.contributor.institutionDivision of Applied Sciences, WCU Program, Gyeongsang National University, Jinju 660-701, South Koreaen
dc.contributor.institutionDepartments of Horticulture and Landscape Architecture, Purdue University, West Lafayette, IN 47907, United Statesen
kaust.authorBressan, Ray Anthonyen
kaust.authorNarasimhan, Meena L.en

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