Leukotrienes (LTs) are known to act as a mediator provoking tissue response in inflammation. LTs, particularly type B4 (LTB4) as chemotactic factor of neutrophil are released from neutrophils and gastric mucosal cells when these cells are stimulated by Helicobacter pylori. The present study was performed to test a possibility that eupatilin may prevent the H. pylori-induced gastric cell damage by observing whether this chemical inhibit the release of LTB4 from H. pylori-stimulated gastric cells (Kato III) and neutrophils. As observed in the previous study, H. pylori induced the release of LTB4 from these cells and at the same influx of Ca2+ into the cells. In the presence of eupatilin, the release of LTB4 was inhibited whereas Ca2+ influx was not affected. Probably eupatilin may inhibit the release of LTB4 by preventing the synthesis of LTs. These results suggest that eupatilin can has a therapeutic effect on H. pylori-induced gasric cell damage.
Helicobacter pylori* ; Helicobacter* ; Inflammation ; Leukotriene B4* ; Leukotrienes ; Neutrophils*

It has been implicated that leukotrienes play roles in the pathogenesis of gastritis and gastric ulceration associated with Helicobacter pylori (H. pylori). Rebamipide is being used as an antiulcer drug but it's mechanism of action has not been understood well. One possible mechanism of action of this drug is to inhibit the cellular release of leukotrienes by various stimuli, particularly H. pylori. In the present study, attempts were made to test this possibility and the results are as follows. When Kato III cells (gastric adenoma cells) were stimulated by H. pylori, leukotriene D4 (LTD4) was released and rebamipide inhibited this release dose-dependently. Similar experiment was performed on neutrophils because the infilteration of neutrophils is a common phenomenon in H. pylori-infected gasrtric tissues. Neutrophils released LTD4 when these cells were stimulated by H. pylori and rebamipide also inhibited this release. Furthermore, rebamipide inhibited the release of LTD from neutrophils induced by calcium ionophore A23187 and arachidonic acid. The results suggest that rebamipide has the action to inhibit the release of LTD4 from various cells and this action may contribute in part to prevent the ulcerogenesis induced by H. pylori.
Adenoma ; Arachidonic Acid ; Calcimycin ; Calcium ; Gastritis ; Helicobacter pylori* ; Helicobacter* ; Leukotriene D4* ; Leukotrienes ; Neutrophils ; Stomach Ulcer

We had experienced a case of congenital lobar emphysema in a 3 months old male infant. Chief symptoms included tachypenea, respiratory difficulty, cyanosis, Chest X-ray or chest CT scan revealed extensive emphysematous changes of the right upper and middle lobes, compression of the right lower lobe and shifted of mediastinum to the left side. This condition was appeared in the absence of infection and foreign body in the bronchus and its failure to respond to conservative treatment. This patient was treated by the right upper and right middle lobes pneumonectomy. A brief review of literature was made.
Bronchi ; Cyanosis ; Emphysema* ; Foreign Bodies ; Humans ; Infant ; Male ; Mediastinum ; Pneumonectomy ; Thorax ; Tomography, X-Ray Computed

This experiment was performed to study the morphological responses of the thymic cortex of the mice after administration of BCG. Healthy adult mice weighing 25gm each were divided into normal and experimental groups. BCG[0.03X108-0.32X108 CFU] were injected subcutaneously to the animals every other day, and animals were sacrificed at 4 days, 1 week, 2 weeks and 8 weeks following the first injection. Thymus were removed immediately after sacrifice and transferred to cold phosphate buffered 2.5% glutaraldehyde-1.5% paraformaldehyde solution[pH 7.3], and cut into small pieces. Tissue samples were fixed for 2-3 hours in the same fixative, postfixed with phosphate buffered 1% osmium tetroxide solution[pH 7.3], dehydrated in a graded series of alcohol, and embedded in araldite mixture. Ultrathin sections stained with uranyl acetate and lead citrate were observed with a JEM 100CX-II electron microscope. The observed results were as follow : 1. In the early BCG treated groups, a few eosinophile leucocytes were observed, but more eosinophils were observed in later groups. Some elongated and bar-shaped lysosomes with eletron lucent gap were often obserced in the macrophages. 2. Cortical population of thymocytes in the thymus were reduced, whereas territoris of the epithelial reticular cells were expanded especially in 2 weeks and 8 weeks groups. Some portion of the thymic cortex exhibited large intercellular spaces, and a few nuclear bodies filled with materials of medium density were observed in the epithelial reticular cells. 3. In the 8 weeks groups, macrophages, plasma cells and eosinopile leucocytes and developing eosinophile leucocytes were often observed in the thymic cortex. Distended cisternae of granular endoplasmic reticula and newly forming prosecretory granulses in the Golgi complex were ovserved in som plasma cells. From the above results, it was suggested that repeated treatment with BCG could induce disturb the maturation and differentiation of the T lymphocytes. In turn, BCG, if repeatedly injected, may disturb the immunological medchanism.
Adult ; Animals ; Citric Acid ; Eosinophils ; Extracellular Space ; Golgi Apparatus ; Humans ; Lysosomes ; Macrophages ; Mice* ; Mycobacterium bovis* ; Osmium Tetroxide ; Plasma Cells ; T-Lymphocytes ; Thymocytes ; Thymus Gland

In this report, the inhibitory action of eupatilin was investigated by using leukotriene D4 in the human neutrophils and Kato III cells (Gastric adenoma cells as a substitute for gastric mucosal cells) stimulated by Helicobacter pylori. Leukotriene D4 (LTD4) was released from both neutrophils and Kato III cells when these cells were incubated with H. pylori. The release of LTD4 increased time-dependently and the maximum release of LTD4 was 2.3-2.5 pmol. But in the presence of eupatilin, the release of LTD4 from these cells was inhibited in a dose-dependent manner. In the neutrophils, die release of LTD4 was suppressed to 70% and 50% of the control levels when neutrophils was incubated with 0.01 and 0.1 mM of eupatilin. In the Kato III cells, the release of LTD4 was suppressed to 59% and 27% of the control levels by adding 0.01 and 0.1 mM of eupatilin. We estimated the intracellular Ca2+ levels when Kato III cells and neutrophils were stimulated by H. pylori using 45Ca. But the suppressive effect of eupatilin on Ca2+ influx into these cells was not significant. We also obtained the results that H. pylori induced Ca2+ influx into these cells by confocal microscopy, however there was no differences in the dose level of eupatilin. These results were confirmed by 1H Nuclear Magnetic Resonance(NMR) spectroscopy. The NMR patterns of eupatilin in the absence of Ca2+ was changed compare with when Ca2+ was present, but its effect was not strong.
Adenoma ; Helicobacter pylori ; Helicobacter* ; Humans* ; Leukotriene D4* ; Microscopy, Confocal ; Neutrophils* ; Spectrum Analysis

Leukotrienes (LTs) are known to act as a mediator provoking tissue response in inflammation. This finding implicates that LTs also play important roles in the pathogenesis of H. pylori-induced gastritis and gastric ulceration. Rebamipide is being currently used as a therapeutics for gastritis and peptic ulcer, but their mechanisms of action have not been known clearly yet. One possibility is that their therapeutic effects are ascribed to interfering with the H. pylori-induced release of LTs from neutrophils and gastric mucosal cells. In the present study, this possibility was tested using LTB4 as the test material in human neutrophils and Kato III cells(gastric adenoma cells as a substitute for gastric mucosal cells). The release of LTB4 from both neutrophils and Kato III cells was time and H. pylori-dose dependent. The maximum release of LTB4 was induced by neutrophils and Kato III cells when these cells incubated with H. pylori 4.8 X 108 cells/ml for 30 min. But in the presence of rebamipide the release of LTB4 from these cells was suppressed in dose dependent manners. The release was completely suppressed at 1.0 mM of rebamipide in neutrophils and 2.0 mM of this drug in Kato III cells, respectively. We also obtained the results that the release of LTB4 was induced by A23187 (Ca2+ ionophore) and the A23187-induced release was also inhibited by rebamipide. It seems that the mechanism of action of rebamipide is through its interaction with the level of intracellular Ca2+. In view of the roles of LTB4 in inflammatory reaction and the roles of H. pylori in gastritis and peptic ulcer, the effects of this drug observed in this study may contribute to their therapeutic action in these gastric disorders.
Adenoma ; Calcimycin ; Gastritis ; Helicobacter pylori* ; Helicobacter* ; Humans ; Inflammation ; Leukotriene B4* ; Leukotrienes ; Neutrophils ; Peptic Ulcer ; Stomach Ulcer