Background-Helicobacter pylori strains possessing the cagA gene are thought to induce interleukin 8 (IL-8) in gastric mucosa. However, it is still unclear whether a relation exists between the cagA gene and the expression patterns of cytokines other than IL-8. Aims-To investigate the relation between the cagA gene and the production of various cytokine proteins using an enzyme linked immunosorbent assay (ELISA). Patients and methods-In 184 patients, the cagA gene was detected by polymerase chain reaction (PCR), and levels of production of IL-1 , IL-6, IL-7, IL-8, IL-10, and tumour necrosis factor (TNF-) in antral biopsy specimens were measured by ELISA. Results-Mucosal levels of IL-1 , IL-6, IL-8, and TNF-were significantly higher in H pylori positive than in H pylori negative patients. Furthermore, the mucosal levels of IL-1 and IL-8 were significantly higher in specimens infected with cagA positive strains than in those infected with cagA negative strains. In H pylori positive patients, the mucosal level of IL-8 was closely correlated with that of IL-1 (p<0.0001), and the mucosal level of IL-6 was closely correlated with that of TNF-(p<0.0001). Conclusion-These findings suggest that the ability to induce cytokines diVers among the strains; cagA + strains induce various kinds of cytokines and may cause severe inflammation, whereas cagA − strains induce IL-8 and IL-1 only weakly and may cause only mild inflammation. However, as most patients infected with the cagA + strains have gastritis, these strains may not be equivalent to ulcerogenic strains. (Gut 1997; 41: 442-451)
Background-Although chemokines have been suggested to play an important role in Helicobacter pylori associated gastritis, few studies have investigated the role of chemokines other than interleukin 8 (IL-8) in gastric mucosa. Aims-To investigate the expression and production patterns of various chemokines using gastric biopsy specimens. Methods-In 192 patients, expression patterns of C-X-C chemokines (IL-8 and growth regulated (GRO )) and C-C chemokines (regulated on activation, normal T cell expressed and presumably secreted (RANTES), monocyte chemotactic and activating factor (MCAF), macrophage inflammatory protein 1 (MIP-1 ), and MIP-1 ) were examined using reverse transcription polymerase chain reaction (RT-PCR) and enzyme linked immunosorbent assay (ELISA). cagA gene was identified using PCR. Results-H pylori infection was associated with increased rates of expression of mRNA for IL-8, GRO , RANTES, and MIP-1 and with increased levels of mucosal IL-8 and GRO . IL-8 and GRO levels correlated with the density of H pylori in both the antrum and corpus. The levels of these chemokines correlated with cellular infiltration in the antrum but not the corpus. cagA gene positive H pylori infection was associated with increased rates of expression of mRNA for IL-8 and GRO and with increased levels of these chemokines. Conclusion-H pylori infection is associated with increased expression rates and production of C-X-C chemokines (IL-8 and GRO ), but not with increased production of C-C chemokines. Although H pylori infection is associated with increased C-X-C chemokines in the antrum and corpus, there is a diVerence in the inflammatory response between these two areas of the stomach. (Gut 1998;42:609-617)
The immune responses to Helicobacter pylori infection play important roles in gastroduodenal diseases. The contribution of gamma interferon (IFN-γ) to the immune responses, especially to the induction of gastric inflammation and to protection from H. pylori infection, was investigated with IFN-γ gene knockout (IFN-γ−/−) mice. We first examined the colonizing abilities of eight H. pylori strains with a short-term infection test in order to select H. pylori strains which could colonize the mouse stomach. Only three strains (ATCC 43504, CPY2052, and HPK127) colonized C57BL/6 wild-type mice, although all of the strains except for ATCC 51110 could colonize IFN-γ−/− mice. The number of H. pyloriorganisms colonizing the stomach in wild-type mice was lower than that in IFN-γ−/− mice. Oral immunization with the CPY2052 sonicate and cholera toxin protected against infection with strain CPY2052 in both types of mouse. These findings suggested that IFN-γ may play a protective role in H. pylori infection, although the degree of its protective ability was estimated to be low. In contrast, in a long-term infection test done to examine the contribution of IFN-γ to gastric inflammation, CPY2052-infected wild-type mice developed a severe infiltration of mononuclear cells in the lamina propria and erosions in the gastric epithelium 15 months after infection, whereas CPY2052-infected IFN-γ−/− mice showed no inflammatory symptoms. This result clearly demonstrated that IFN-γ plays an important role in the induction of gastric inflammation caused by H. pylori infection.
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