Rat gastric mucosal cells express ICAM-1 and proinflammatory cytokines during indomethacininduced mucosal injury

Okada, Akihiko; Kinoshita, Yoshikazu; Waki, Shinya; Fukui, Hirokazu; Maekawa, Toru; Matsushima, Yumi; Kawanami, Chiharu; Kishi, Kiyohiko; Nakata, Hirohisa; Wang, He Yao; Hassan, Masriana; Chiba, Tsutomu

doi:10.1016/s0022-2143(98)90062-2

Cited by 25 publications

(14 citation statements)

References 18 publications

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“…The present study indicated that TNF-α and IL-1β mRNA were detected only weakly in intact gastric mucosa, but were significantly upregulated in the gastric tissues of indomethacin-treated rats. These results are consistent with those of the previous studies that mucosal pro-inflammatory cytokines, such as, TNF-α and IL-1β play important roles in the activation and infiltration of leukocytes associated with NSAID-induced gastric damage (Santucci et al, 1994(Santucci et al, , 1995Okada et al, 1998;Shimizu et al, 2000). Furthermore, Pretreatment of QGC inhibited increases in the expressions of TNF-α and IL-1β mRNA in the damaged gastric tissues of indomethacin-treated rats.…”

Section: Discussionsupporting

confidence: 92%

“…It is well known that the pathogenesis of NSAIDs-induced gastrointestinal damage is related to the suppression of prostaglandin synthesis due to their directly blocking cyclooxygenase activity (Wallace, 2001). In addition, oxygen radical and proinflammatory cytokine such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β released from activated neutrophils are involved in the pathogeneses of a variety of gastric injuries, including those caused by NSAIDs (Yoshikawa et al, 1993;Okada et al, 1998;Kwiecien et al, 2003;Whittle, 2003). Moreover, TNF-α and IL-1β markedly upregulate the intercellular adhesion molecule-1 (ICAM-1) as an indicator of neutrophil and macrophage infiltration into scarred mucosa when gastric ulcers recur (Wallace et al, 1993;Andrews et al, 1994;Watanabe et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

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The effect of quercetin-3-O-β-D-glucuronopyranoside on indomethacin-induced gastric damage in rats via induction of mucus secretion and down-regulation of ICAM-1 expression

et al. 2011

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The mechanism of the protective effect of quercetin-3-O-β-D-glucuronopyranoside (QGC) from the leaves of Rumex aqauticus on indomethacin (IND, a representative NSAID)-induced gastric damage in rats was investigated. Pre-treatment with QGC significantly attenuated IND-induced gastric mucosal injury. An increase in myeloperoxidase (MPO) activity and expression of intercellular adhesion molecule (ICAM)-1 protein and mRNA expression of the pro-inflammatory cytokines tumor necrosis factor-α and interleukin-1β, as well as a decrease in gastric mucus secretion were detected in the gastric mucosa of IND-treated rats. QGC reversed the side effect of IND on MPO activity and mucus production. Furthermore, QGC pre-treatment notably decreased ICAM-1 protein and mRNA expression of the pro-inflammatory cytokines, suggesting that QGC protection from IND-induced damage is associated with increased gastric mucus secretion, inhibition of free radical production by activated neutrophils via ICAM-1, and pro-inflammatory cytokine downregulation.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

The effect of quercetin-3-O-β-D-glucuronopyranoside on indomethacin-induced gastric damage in rats via induction of mucus secretion and down-regulation of ICAM-1 expression

et al. 2011

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“…Mucosal inflammation activates leukocytes in the gastric wall, which release immunoregulatory cytokines such as interleukin (IL)-1, IL-6, IL-8, and tumor necrosis factor (TNF)-α [28][29][30][31], while nitric oxide (NO) production also increases due to induction of NO synthase [32]. Some of these cytokines are known to interfere with gastrointestinal motility [33][34][35][36], while NO inhibits gastric emptying and antral motility [37].…”

Section: Discussionmentioning

confidence: 99%

Oral Erythromycin Accelerates Impaired Gastrointestinal Motility After Endoscopic Mucosal Resection

et al. 2007

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Gastrointestinal motility may be impaired after endoscopic mucosal resection of gastric lesions. We investigated whether oral erythromycin could improve motility. Twenty patients were divided randomly into groups that received oral omeprazole with or without erythromycin. Motility was recorded overnight at 3 days before and 4 days after endoscopic resection using a microtransducer probe. In the group without erythromycin, gastric phase III activity decreased significantly after endoscopic resection, while it was increased significantly by erythromycin (P < 0.01). After resection, there were significantly more gastric phase III events in the erythromycin group (P < 0.05). The interval between the start of the evening meal and the initial gastric phase III activity was significantly prolonged after resection, while this interval was significantly shortened by erythromycin (P < 0.05). The gastric phase III cycle length was also significantly shortened by erythromycin (P < 0.05). Postprandial and fasting gastrointestinal motility were impaired after endoscopic resection, and postprandial as well as fasting motility were improved by oral erythromycin.

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“…They also found that antibodies against the adhesion molecules ICAM-1 and to a lesser extent P-selectin reduced both mucosal injury and leukocyte adherence in the rat (25). Indomethacin has been shown to elevate the level of expression of both ICAM-1 and P-selectin (17,18). Furthermore, depletion of circulating neutrophils with specific antiserum significantly reduced NSAID-induced injury in both the rat stomach (24) and small bowel (3).…”

mentioning

confidence: 94%

Transmural gradient of leukocyte-endothelial interaction in the rat gastrointestinal tract

Perry¹,

Phillipson²,

Holm³

2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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-Gastrointestinal injury usually starts in the superficial mucosa. We investigated whether leukocyteendothelial interactions were greater in the gastrointestinal mucosa than the submucosa and muscularis in control tissue and after upregulation of adhesion molecules with endotoxin and after chemical insult with nonsteroidal anti-inflammatory drugs. Inactin-anesthetized rats were given either endotoxin, flurbiprofen, or nitric oxide (NO)-flurbiprofen, after which ICAM-1 and P-selectin expression was measured with the dual-label antibody technique. Leukocyte-endothelial interactions in the different gastric layers were assessed after endotoxin using intravital microscopy. Endotoxin caused a two-to threefold increase in ICAM-1 expression in the stomach and duodenum. There was, however, a gradient in expression across the gut wall with the level of expression in the superficial mucosa (per g) being only 10 -25% of that in the deeper layers in both control and endotoxin-treated animals. Constituitive expression of P-selectin in control animals was barely detectable. Endotoxin caused a modest increase in mucosal P-selectin but a very significant increase in the deeper layers. Flurbiprofen caused a slight upregulation of ICAM-1 in the gastric mucosa and duodenum, whereas NO-flurbiprofen had no affect on expression. Intravital microscopy revealed no adhesion and virtually no leukocyte rolling in the vessels of the gastric mucosa despite endotoxin treatment. There was, however, some adhesion and significant leukocyte rolling in the submucosa and muscularis. Thus the superficial gastric and duodenal mucosal microcirculations have a much lower density of ICAM-1 and P-selectin and less leukocyteendothelial interactions than occurs in the deeper layers of the gut wall even during stimulated upregulation with endotoxin. intracellular adhesion molecule 1; P-selectin; endotoxin; flurbiprofen; intravital microscopy MANY FORMS of gastrointestinal injury such as that caused by ischemia-reperfusion or nonsteroidal anti-inflammatory drugs (NSAID) are initiated by erosion of the superficial mucosa. Leukocytes appear to play a key role in these forms of injury (7,9,(23)(24)(25). Smith et al. (21) showed that ischemiareperfusion induced gastric mucosal erosion and bleeding in the rat. This injury was largely prevented when circulating neutrophils were depleted with antiserum. In the cat, administration of antibodies against leukocyte adhesion prevented the increase in mucosal permeability and net fluid secretion observed in the small bowel after ischemia-reperfusion (13).The NSAID indomethacin can cause severe mucosal injury. Asako et al. (1) demonstrated that clinically relevant concentrations of indomethacin induced leukocyte rolling and adhesion (but not emigration) through an leukotriene B4 (LTB4)-dependent mechanism. Wallace and co-workers then showed that the gastric injury induced by indomethacin in both the rat (25) and rabbit (23) could be markedly reduced by immunoneutralization of the adhesion molecule CD11/CD18. They also f...

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Rat gastric mucosal cells express ICAM-1 and proinflammatory cytokines during indomethacininduced mucosal injury

Cited by 25 publications

References 18 publications

The effect of quercetin-3-O-β-D-glucuronopyranoside on indomethacin-induced gastric damage in rats via induction of mucus secretion and down-regulation of ICAM-1 expression

The effect of quercetin-3-O-β-D-glucuronopyranoside on indomethacin-induced gastric damage in rats via induction of mucus secretion and down-regulation of ICAM-1 expression

Oral Erythromycin Accelerates Impaired Gastrointestinal Motility After Endoscopic Mucosal Resection

Transmural gradient of leukocyte-endothelial interaction in the rat gastrointestinal tract

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