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  • 1
    ISSN: 1573-2568
    Keywords: H. PYLORI ; MONGOLIAN GERBIL ; GASTRIC MUCOSAL LESIONS ; INFLAMMATION ; MYELOPEROXIDASE ; NEUTROPHIL CHEMOTAXIS
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined pathological changes in theformation of Helicobacter pylori-induced gastric lesionsin Mongorian gerbils. H. pylori (NCTC11637) was orallyadministered once to the animals and was detected in the gastric mucosa of all gerbils given thebacteria. The number of viable H. pylori increasedduring the initial two weeks and thereafter reached aplateau level. The initial pathological changes were found at one week, ie, edema/congestion and awhite viscous substance only in the antrum. At twoweeks, superficial damage appeared in the antrum,although inflammatory cell infiltration had notoccurred. Gastritis with lymphoid follicles was observedin the antrum and fundus from three weeks. At fourweeks, mucosal lesions were detected as a fewhemorrhagic spots in the fundus adjacent to the antrum.In the control animals, however, no pathologicalchanges were observed even at four weeks. In the gastricmucosa infected with H. pylori , myeloperoxidaseactivity was negligible at two weeks, but was extremely elevated at four weeks. Similarly, neutrophilchemotactic activity was only slightly increased at twoweeks, but was markedly elevated at four weeks. Theseresults indicate that H. pylori infection induces initial pathological changes only in theantrum, but mucosal lesions occur in the fundus adjacentto the antrum. Furthermore, it is demonstrated that theinitial superficial damage is generated by factors other than chemokines and neutrophil-associatedfactors, although mucosal inflammation may contribute tothe subsequent formation of lesions andulcers.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-2568
    Keywords: INTERLEUKIN-1β ; GASTRIC EPITHELIAL CELL ; GROWTH FACTOR ; WOUND REPAIR ; RGM1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined the effect of interleukin-1β(IL-1β) on spontaneous and enhanced restoration(cell migration and proliferation) using an in vitrowound model comprising a confluent monolayer of ratgastric epithelial RGM1 cells. Repair of an artificialwound in a cell monolayer was found to be time- andconcentration-dependent when the cells were incubatedwith epidermal growth factor (EGF) or transforming growth factor (TGF)-α alone for up to 24hr. The growth factors also stimulated DNA synthesissignificantly for 24 hr in a concentration-relatedmanner. IL-1β had no effect on wound restoration in the absence of the growth factors. However, itmarkedly inhibited the restoration enhanced by EGF andTGF-α, the inhibition being about 60% and 70%,respectively. In addition, IL-1β significantly reduced the DNA synthesis stimulated by thegrowth factors. The EGF- and TGF-α-enhancedrestoration was reduced by about 30% by mitomycin C,which potently inhibited the stimulated DNA synthesis.Mitomycin C had no effect on the spontaneous restoration.Even when treated with mitomycin C, the inhibitoryeffect of IL-1β on the enhanced wound repair wasstill observed; however, the extent of the inhibition was decreased. These results indicate thatIL-1β inhibits the migration as well as theproliferation of gastric epithelial cells enhanced byEGF and TGF-α, resulting in a failure of woundhealing.
    Type of Medium: Electronic Resource
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