| [ Background&Objective ] Helicobacter pylori(H.pylori) is a gram-negativebacterium that chronically colonizes the gastric mucosa of humans, causing chronicgastritis, peptic ulcer, and in some individuals gastric adenocarcinoma and B-celllymphoma of mucosa-associated lymphoid tissue(MALT). The pathogenesis ofH.pylori is complex and was not completely understood. Several pathogenic factor ofH.pylori, including the adherence factor, lipopolysaccharides(LPS), flagella, urease,vaculating cytotoxin(VacA) and cytotoxin-associated protein(CagA) may contributeto the pathogenesis of H.pylori-induced lesions. It is well known that the infection ischaracterized by a massive infiltration of the gastric mucosa with neutrophils andlymphocytes. The infection results in dramatically increased mumber of H.pylori-specific antibody secreting cells(ASCs) in human mucosa. Furthermore, theinfection usually induces high levels of H.pylori-specific antibodies in serum, andsignificant antibody levels have also been demonstrated in saliva, gastric juice, andfeces. Recent study reveal that interleukin-8(IL-8), a neutrophil chemotactic factorbelonging to CXC family of chemokines, has also influence development of gastricdisease. Despite a vigorous humoral/inflammatory response against H.pyloriantigens(Ag), most infected subjects fail to eliminate the pathogen spontaneously andthe infection is usually lifelong. In recent years, evidence has accumulated to suggestthat in both human patients and animal models, host cellular immune response is animportant determinant of the outcome of infection. To date all of the studies on cellular immune responses to H.pylori have been performed in humans and the nature of Ag-specificn T cell-madiated responses has not been well defined. In particular the T lymphocyte subset CD4+/CD8+ and Thl/Th2 responses in H.pylori infection and how these responses may contribute to immunity versus disease remains different viewpoint. Little is known about the cellular immune responses to H.pylori infected children. Since most infections with H.pylori occur during childhood and the immunity between children and adult may be different. It is worthwhile to understand the T lymphocyte responses in natural infection with H.pylori in children. For this reason, the changes of gastric mucosal and peripheral blood T lymphocyte subsets in H.pylori infected children with gastritis and duodenal ulcer have been investigated in this study in order to provide preliminary date for clarificating the immunopathogenesis of children infecion with H.pylori. (Methods] Eighty nine patients with digestive symptoms were assessed by endoscopy examination, rapid urease test, histology and culture, and there were eight patients with H.pylori negative normal mucosa(H.pylori Nor), twenty seven patients with H.pylori negative chronic superficial gastritis(H.pylori CSG), forty four patients with H.pylori positive chronic superficial gastritis(/H.pylori +CSG) and ten patients with H.pylori positive duodenal ulcer(H.pylori +DU). Gastric biopsy specimens were obtained from each patient. Peripheral blood samples were obtained from thirty eight patient(twelve patients with H.pylori+ CSG, five patients with H.pylori+ DU and twenty one patients were H.pylor negative). H.pylori infection was identified by rapid urease test, histology and culture. Culture positive or at least two of those positive was considered to be H.pylori infected. Four gastric antrum mucosa specimens were placed in Hanks's balanced salt solution containing 1 mM dithiothreitol(DTT) and 1 mM ethylenediamine tetraacetic acid(EDTA). The specimens were agitated for one hour at 37 and washed three times with RPMI 1640 after removing the epithelial layer, and then treated with collagenase, type I(120u/ml) for three hours at 37 with agitation. The mononuclear cells(MNCs) were collected by means of removing undigested material and washed three times with RPMI 1640. Isolated gastic... |
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