Takaya Iida

Real-time monitoring of trans-epithelial electrical resistance in cultured intestinal epithelial cells: the barrier protection of water-soluble dietary fiber

In this study we aimed to verify a real‐time trans‐epithelial electrical resistance (TEER) monitoring system in a Caco‐2 monolayer and to investigate the therapeutic effect of partially hydrolyzed guar gum (PHGG), a dietary fiber, against interferon (IFN)‐γ‐induced intestinal barrier dysfunction using this monitoring system.

Rapamycin Improves Mortality Following Intestinal Ischemia-Reperfusion via the Inhibition of Remote Lung Inflammation in Mice.

Background/Aims: Acute-phase intestinal ischemia-reperfusion (I-R) injury can result in multiple organ failure, which may sometimes be fatal. However, no reliable treatment for this clinical state is available. Rapamycin has been reported to protect heart, brain and kidney against I-R injury. The aim of this study was to examine whether rapamycin could protect mice against I-R-induced intestinal and remote organ injury. Methods: Ischemia was induced in the intestine of C57BL/6 mice by occluding the superior mesenteric artery for 1 h. Mice received rapamycin at a dose of 5 mg/kg or vehicle by the intraperitoneal injection 1 h before ischemia. The survival rate, inflammatory responses in the intestine and the lung, bacteria cultured from lung tissue and the phagocytic capacity of alveolar macrophages were examined. Results: Treatment with rapamycin improved survival rate after intestinal I-R. Histological and biochemical parameters of I-R-induced intestinal injury/inflammation were similar in both rapamycin-treated and untreated mice. However, signs of lung injury/inflammation were significantly attenuated in rapamycin-treated mice compared to control mice. The reduction of lung bacteria and the increase in phagocytic activity were accompanied in mice treated with rapamycin. Conclusion: Rapamycin improved mortality following intestinal I-R via the inhibition of remote lung inflammation in mice.

Tu1996 Rapamycin Reduced the Mortality in Mice Injured by Intestinal Ischemia-Reperfusion Through the Inhibition of Remote Organ Failure

Rapamycin Reduced the Mortality in Mice Injured by Intestinal IschemiaReperfusion Through the Inhibition of Remote Organ Failure Takaya Iida, Yuji Naito, Tomohisa Takagi, Kazuhiro Katada, Katsura Mizushima, Yasuki Higashimura, Syunsuke Kishimoto, Kentaro Suzuki, Hideki Horie, Wataru Fukuda, Yutaka Inada, Yukiko Uehara, Munehiro Kugai, Hiroyuki Yoriki, Toshifumi Tsuji, Akifumi Fukui, Kazuhiro Kamada, Kazuhiko Uchiyama, Osamu Handa, Nobuaki Yagi, Toshikazu Yoshikawa

Su2063 Partially Hydrolyzed Guar Gum (PHGG) Inhibits Castor Oil-Induced Diarrhea in Rats Through the Inhibition of Substance P Production

Partially Hydrolyzed Guar Gum (PHGG) Inhibits Castor Oil-Induced Diarrhea in Rats Through the Inhibition of Substance P Production Kentaro Suzuki, Yuji Naito, Kazuhiro Kamada, Syunsuke Kishimoto, Yukiko Uehara, Hideki Horie, Wataru Fukuda, Yutaka Inada, Takaya Iida, Munehiro Kugai, Toshifumi Tsuji, Hiroyuki Yoriki, Akifumi Fukui, Yasuki Higashimura, Katsura Mizushima, Kazuhiro Katada, Kazuhiko Uchiyama, Osamu Handa, Tomohisa Takagi, Nobuaki Yagi, Zenta Yasukawa, Makoto Tokunaga, Tsutomu Okubo, Lekh R. Juneja, Toshikazu Yoshikawa

Mo1823 Involvement of MDR1 in Intestinal Epithelial Injury Caused by Acetylsalicylic Acid

Introduction Intestinal fibrosis (IF) is a major complication of chronic inflammation of the intestinal tissue in inflammatory bowel disease (IBD). IF can cause narrowing of the intestinal lumen, which may lead to stricture formation. Currently, adequate models are lacking to study the mechanism of intestinal fibrosis in IBD. Our aim is to develop an ex vivo model for IF by using mouse precision-cut intestinal slice (PCIS). In addition, regional differences in the onset of fibrosis in the bowel will be studied. In PCIS all cell types are present in their original tissue-matrix environment. As fibrosis is a multicellular phenomenon, PCIS can be used as a model to study the early onset of intestinal fibrosis. Methods Mouse jejunum, ileum and colon were excised and prepared as segments embedded in agarose. PCIS (estimated 300-400 μm) were prepared and incubated up to 48 hr. ATP content of the PCIS was used to assess the general viability. To study the early onset of fibrosis, the gene expression of different fibrosis markers: Pro-Collagen 1 A1 (COL1A1), Heat Shock Protein 47 (HSP47), alpha-Smooth Muscle Actin (SMA) and Fibronectin (FN1) was determined in PCIS after 48 hr of incubation. Results Mouse PCIS from the different regions of the bowel were viable up to 48 hr in culture. After 48 hr of incubation of PCIS, HSP47 and FN1 gene expression was significantly up-regulated, compared to PCIS directly after slicing, in jejunum (3.9 and 3.6 fold, respectively) and in ileum (4.5 and 4.9 fold, respectively). Gene expression of Col1A1 (0.7 fold) was only down-regulated in PCIS from the colon. SMA gene expression was down-regulated in PCIS from all the regions of the intestine. PCIS from jejunum cultured in the presence of 5ng/mL Transforming-Growth Factor (TGF)β1 for 48 hr, HSP47 (1.2 fold), FN1 (4.6 fold) and COL1A1 (2.0 fold) were significantly upregulated compared to control PCIS after 48 hr of incubation. In addition, in PCIS from Ileum incubated with 5ng/mL TGF-β1, the gene expression of HSP47 (1.9 fold) and FN1 (3.9 fold) was significantly increased. In PCIS from the colon cultured for 48 hr in the presence of 5ng/ml TGF-β1, the gene expression of fibrosis markers was not affected. Conclusion Mouse PCIS from different regions of the bowel can successfully be cultured for 48 hr. Fibrosis markers are induced by incubation up to 48 hr and by addition of TGFβ1 in jejunum and ileum PCIS, but not in colon PCIS. We are the first to show that regional differences in the onset of intestinal fibrosis can be measured using PCIS.