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

Violeta Arsenescu, Meena L. Narasimhan, Tuna Halide, Ray A. Bressan, Chiara Barisione, Donald A. Cohen, Willem J.S. De Villiers, Razvan Arsenescu

Research output: Contribution to journalArticle

22 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)2818-2832
Number of pages15
JournalDigestive Diseases and Sciences
Volume56
Issue number10
DOIs
StatePublished - Oct 1 2011
Externally publishedYes

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Adiponectin
Colitis
Interleukin-10
Dendritic Cells
Cytokines
Arginase
Peroxisome Proliferator-Activated Receptors
Osteopontin
Adipokines
Chemotactic Factors
Angiotensins
Tretinoin
Interleukin-1
Inbred C57BL Mouse
Inflammatory Bowel Diseases
Crohn Disease
Hypertrophy
Disease Progression
Cell Survival
Histology

All Science Journal Classification (ASJC) codes

  • Physiology
  • Gastroenterology

Cite this

Arsenescu, Violeta ; Narasimhan, Meena L. ; Halide, Tuna ; Bressan, Ray A. ; Barisione, Chiara ; Cohen, Donald A. ; De Villiers, Willem J.S. ; Arsenescu, Razvan. / Adiponectin and plant-derived mammalian adiponectin homolog exert a protective effect in murine colitis. In: Digestive Diseases and Sciences. 2011 ; Vol. 56, No. 10. pp. 2818-2832.
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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.",
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Arsenescu, V, Narasimhan, ML, Halide, T, Bressan, RA, Barisione, C, Cohen, DA, De Villiers, WJS & Arsenescu, R 2011, 'Adiponectin and plant-derived mammalian adiponectin homolog exert a protective effect in murine colitis', Digestive Diseases and Sciences, vol. 56, no. 10, pp. 2818-2832. https://doi.org/10.1007/s10620-011-1692-0

Adiponectin and plant-derived mammalian adiponectin homolog exert a protective effect in murine colitis. / Arsenescu, Violeta; Narasimhan, Meena L.; Halide, Tuna; Bressan, Ray A.; Barisione, Chiara; Cohen, Donald A.; De Villiers, Willem J.S.; Arsenescu, Razvan.

In: Digestive Diseases and Sciences, Vol. 56, No. 10, 01.10.2011, p. 2818-2832.

Research output: Contribution to journalArticle

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T1 - Adiponectin and plant-derived mammalian adiponectin homolog exert a protective effect in murine colitis

AU - Arsenescu, Violeta

AU - Narasimhan, Meena L.

AU - Halide, Tuna

AU - Bressan, Ray A.

AU - Barisione, Chiara

AU - Cohen, Donald A.

AU - De Villiers, Willem J.S.

AU - Arsenescu, Razvan

PY - 2011/10/1

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N2 - 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.

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