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Cilostazol, a specific PDE-3 inhibitor, ameliorates chronic ileitis via suppression of interaction of platelets with monocytes.

Authors
  • Matsunaga, Hisayuki
  • Hokari, Ryota
  • Higashiyama, Masaaki
  • Kurihara, Chie
  • Okada, Yoshikiyo
  • Watanabe, Chikako
  • Komoto, Shunsuke
  • Nakamura, Mitsuyasu
  • Kawaguchi, Atsushi
  • Nagao, Shigeaki
  • Miura, Soichiro
Type
Published Article
Journal
AJP Gastrointestinal and Liver Physiology
Publisher
American Physiological Society
Publication Date
Dec 01, 2009
Volume
297
Issue
6
Identifiers
DOI: 10.1152/ajpgi.00240.2009
PMID: 19815627
Source
Medline
License
Unknown

Abstract

Excessive migration of monocytes to a site of intestinal inflammation contributes to tissue damage in Crohn's disease. It is known that cilostazol, a specific phosphodiesterase-3 (PDE-3) inhibitor of platelets, decreases monocyte recruitment to intestinal mucosa through suppression of platelet-monocyte interactions. The objective of this study was to clarify whether cilostazol ameliorates murine ileitis by suppression of monocyte migration. Significant inflammation was induced in the ileum of SAMP1/Yit mice at 23 wk of age after piroxicam treatment for 3 wk. Weight of the terminal ileum of mice was significantly greater with inflammatory cell infiltration in SAMP1/Yit mice than in control mice (AKR-J). Treatment of SAMP1/Yit mice with cilostazol-containing food (200 ppm) for 3 wk significantly attenuated the increase in intestinal weight and the histological changes, including invasion of F4/80-positive macrophages. A significant increase in migration of monocytes and platelets to microvessels of the ileal mucosa was observed in SAMP/Yit mice in vivo by using an intravital fluorescence microscope. Pretreatment with cilostazol significantly attenuated the increased migration of monocytes, possibly through suppression of platelet-monocyte interactions. In conclusion, a PDE-3 inhibitor ameliorates murine ileitis through attenuating migration of monocytes to the intestinal mucosa, suggesting a potential usefulness of antiplatelet drugs for treatment of Crohn's disease.

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