Resistance of germfree rats to indomethacin-induced intestinal lesions

Robert, André; Asano, Tomoaki

doi:10.1016/0090-6980(77)90178-2

Cited by 299 publications

(169 citation statements)

References 7 publications

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“…Several prostaglandins and plant extract (Goulart et al, 2005) also protect the animals against the damages induced by indomethacin. There is hypothesis that certain prostaglandins may protect the mucosal membrane, creating a "cytoprotection" by preventing the spread of microorganisms and/or their toxins through the intestinal wall (Robert and Asano, 1977). In the present study, the microorganism culture study confirmed a growth of E. coli as much in the bacterial culture of the content of the peritonitis as of the intestinal content of the animals that received 8.40 mg/kg of indomethacin.…”

Section: Discussionsupporting

confidence: 68%

“…The microvacuolization of hepatocytes, a suggestive factor of cytoplasmic glycogen increase, the minimal inflammatory infiltrated in the portal triad, and binucleated hepatocyte increase verified at 8.40 mg/kg of indomethacin dose would be not associated to sign of hepatoxicity or hypersensibility of the drug. The post mortem analysis showed that the pregnant rats that received 8.40 mg/kg presented peritonitis and ulcer formation in the colon with adherence to the epiplon, as also observed by other authors (Robert and Asano, 1977;Rodrigues et al, 1986;Yamagiwa et al, 2001). This could promote the embryonic implantation impairment, increasing the preimplantation loss.…”

Section: Discussionsupporting

confidence: 57%

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Effect of indomethacin on the pregnant rat

Damasceno

Volpato

Ferrari

et al. 2008

Braz. arch. biol. technol.

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Section: Discussionsupporting

confidence: 68%

Section: Discussionsupporting

confidence: 57%

Effect of indomethacin on the pregnant rat

Damasceno

Volpato

Ferrari

et al. 2008

Braz. arch. biol. technol.

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“…Evidence for the role of the bacterial flora in the induction of experimental colitis is that germ-free or specific pathogen-free animals develop no or less severe inflammation. This was shown in several colitis models, such as indomethacin-induced colitis [11], HLA-B27 transgenic rats [12], IL-2 knockout mice [2] and IL-10 knockout mice [13]. Recently, Brandwein et al [14] showed that C3H/HeJBir mice, which spontaneously develop colitis, produce antibodies to bacterial antigens of the enteric flora.…”

Section: Introductionmentioning

confidence: 98%

CD4+ T cells from 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis rodents migrate to the recipient's colon upon transfer; down-regulation by CD8+ T cells

Palmen

Wijburg

Kunst

et al. 1998

Clinical and Experimental Immunology

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SUMMARYCD4 þ T cells play an important role in the aetiology of inflammatory bowel disease (IBD), but it is not clear which factor(s) cause activation of these cells. The aim of this study was to examine the effects of adoptive transfer of splenic (CD4 þ ) T cells from TNBS/ethanol-sensitized donor rats to naive recipients and the migration pattern of transferred T cells. For the transfer experiments, colitis was induced in rats by colonic administration of TNBS/ethanol. Seventeen days later, either total splenic T cells or CD4 þ , or CD8 þ T cells were transferred to naive recipients. At days 1, 2 and 3 after transfer, the recipients were killed and the migration pattern of the transferred T cells was studied, as well as inflammatory cells in several organs, including the colon. To determine cytokine profiles of the T cells, colitis was induced in mice. Therefore, different combinations of 2,4-dinitrobenzene sulfonic acid (DNBS) in ethanol or saline, or ethanol alone were intrarectally administered. At day 9 after induction of colitis, mice were killed and cytokine profiles in the colon were studied by reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry. The results show that CD4 þ T cells from donor rats with TNBS/ ethanol-induced colitis migrate in particular to the colon upon transfer to naive recipients, and that this process is down-regulated by CD8 þ T cells. This migration is probably caused by T cell recognition of the colonic bacterial flora and initiates an inflammatory reaction in the recipient's colon, characterized by an increase of the recipient's own T cells, macrophages, and neutrophils. In the mice experiments we showed that a second administration of DNBS/ethanol or ethanol alone, which presumably causes bacterial translocation, results in increased numbers of T cells into the colon, accompanied by an increase in Th1 cytokines. These data suggest that Th1 cells recognize the colonic bacterial flora.

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“…Pathogenesis of small intestinal mucosal injury caused by NSAIDs and aspirin PG is involved in regulation of gastrointestinal blood flow and various mucosal functions such as increasing mucus secretion. The decrease in PG production is considered to be the main cause of small bowel injuries due to NSAIDs [20][21][22][23][24]. In a rat study, exogenous PG administration was reported to markedly inhibit small bowel injuries induced by indomethacin, an NSAID [25].…”

Section: Present Status Of Small Intestinal Mucosal Injury Caused By mentioning

confidence: 99%

Present status and strategy of NSAIDs-induced small bowel injury

et al. 2009

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Non-steroidal anti-inflammatory drugs (NSAIDs) are well known to cause gastroduodenal mucosal lesions as an adverse effect. Recently, the serious problem of NSAID-induced small intestinal damage has become a topic of great interest to gastroenterologists, since capsule endoscopy and balloon enteroscopy are available for the detection of small intestinal lesions. Such lesions have been of great concern in clinical settings, and their treatment and prevention must be devised as soon as possible. The prevalence of NSAIDs-induced small intestinal injury is higher than had been expected. Recent studies show that more than 50% of patients taking NSAIDs have some mucosal damage in the small intestine. The gross appearance of NSAIDinduced enteropathy varies, appearing variously as diaphragm-like strictures, ulcers, erosions, and mucosal redness. To investigate NSAID-induced enteropathy, and to rule out other specific enteropathies, other useful methods (in addition to capsule endoscopy and balloon enteroscopy) include such modalities as radiological examination of the small intestine, the permeability test, scintigraphy or the fecal excretion test using 111 Indium-labeled white blood cells, and measurement of the fecal calprotectin concentration. Diaphragm-like strictures and bleeding from mucosal breaks may be treatable with interventional enteroscopy. Misoprostol, metronidazole, and sulfasalazine are frequently used to treat NSAID-induced enteropathy, but have undesirable effects in some cases. In the experimental model, we confirmed that several existing drugs for gastroduodenal ulcers prevented indomethacin-induced small intestinal injury. Such drugs may be useful for preventing the adverse effects of NSAIDs not only in the stomach but also in the small intestine. We hope to examine these drugs in future clinical studies.

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Resistance of germfree rats to indomethacin-induced intestinal lesions

Cited by 299 publications

References 7 publications

Effect of indomethacin on the pregnant rat

Effect of indomethacin on the pregnant rat

CD4+ T cells from 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis rodents migrate to the recipient's colon upon transfer; down-regulation by CD8+ T cells

Present status and strategy of NSAIDs-induced small bowel injury

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