Helicobacter pylori (HP) infection is a global problem that affects about half of the world’s population and requires sufficient attention in clinical and scientific work. Due to differences in economic and medical c...Helicobacter pylori (HP) infection is a global problem that affects about half of the world’s population and requires sufficient attention in clinical and scientific work. Due to differences in economic and medical conditions among countries around the world, there is currently no unified treatment plan for anti-HP. In China, empirical quadruple therapy is mainly used. With the abuse of antibiotics, many patients face the problem of secondary eradication after failure, and the resistance rate of HP is gradually increasing. After eradication failure, drug sensitivity cultivation is carried out to choose sensitive antibiotics for treatment. A new strategy is currently needed to address how to improve the eradication rate of HP during the first eradication. This article aims to discuss the first-line treatment plans and research progress for eradicating HP based on drug sensitivity testing before eradication. Compared with traditional empirical therapies, treatment based on drug sensitivity results can effectively improve the eradication rate of HP, and reduce drug resistance rates, and adverse reactions, among other benefits. .展开更多
Helicobacter pylori （Hp） infection is the major causative agent of gastric cancer, one of the most common malignant tumors in China. However, there is no consensus on the role of Hp infection in gastric cancer. This...Helicobacter pylori （Hp） infection is the major causative agent of gastric cancer, one of the most common malignant tumors in China. However, there is no consensus on the role of Hp infection in gastric cancer. This review summarizes the role of Hp infection in the development of gastric cancer and its potent molecular mechanisms. The immunological drift of helper T lymphocyte mediated specific immune response after Hp infection is a key of carcinogenesis. This process was adjusted by the ratio of INF-γ and IL-4. Nucleotide-binding oligomerization domain 1 and 2 proteins mediate the activation of innate immune response followed by the activation of NF-κB signaling pathways, exhibiting protective effects against Hp infection. Disrupting the dynamic balance between oncogenes and tumor suppressor genes after exposure to Hp infection may promote the transformation of normal epithelial cells into malignant cells. The levels of transforming growth factor （TGF） β1 and epithelial growth factor （EGF） in Hp positive gastric cancer are higher than those in Hp negative gastric cancer. High level of EGF receptor （EGFR） binds to ligand of EGF or TGF and activates tyrosine kinase, thereby promotes tumor cells proliferation. Simultaneously, tumor cells secrete EGF and TGF and stimulate EGFR overexpression, forming a vicious circle. There is also emerging evidence that the two important angiogenic factors, vascular endothelial growth factor and midkine, are correlated with Hp infection. Hp infection was positively correlated with the activation of p-STAT3, thereby up-regulating the levels of Mcl-1, survivin, Bcl-2, Bcl-xL Cyclin D1 and VEGF and other target protein and regulating tumor cells proliferation and apoptosis.展开更多
文摘Helicobacter pylori (HP) infection is a global problem that affects about half of the world’s population and requires sufficient attention in clinical and scientific work. Due to differences in economic and medical conditions among countries around the world, there is currently no unified treatment plan for anti-HP. In China, empirical quadruple therapy is mainly used. With the abuse of antibiotics, many patients face the problem of secondary eradication after failure, and the resistance rate of HP is gradually increasing. After eradication failure, drug sensitivity cultivation is carried out to choose sensitive antibiotics for treatment. A new strategy is currently needed to address how to improve the eradication rate of HP during the first eradication. This article aims to discuss the first-line treatment plans and research progress for eradicating HP based on drug sensitivity testing before eradication. Compared with traditional empirical therapies, treatment based on drug sensitivity results can effectively improve the eradication rate of HP, and reduce drug resistance rates, and adverse reactions, among other benefits. .
文摘Helicobacter pylori （Hp） infection is the major causative agent of gastric cancer, one of the most common malignant tumors in China. However, there is no consensus on the role of Hp infection in gastric cancer. This review summarizes the role of Hp infection in the development of gastric cancer and its potent molecular mechanisms. The immunological drift of helper T lymphocyte mediated specific immune response after Hp infection is a key of carcinogenesis. This process was adjusted by the ratio of INF-γ and IL-4. Nucleotide-binding oligomerization domain 1 and 2 proteins mediate the activation of innate immune response followed by the activation of NF-κB signaling pathways, exhibiting protective effects against Hp infection. Disrupting the dynamic balance between oncogenes and tumor suppressor genes after exposure to Hp infection may promote the transformation of normal epithelial cells into malignant cells. The levels of transforming growth factor （TGF） β1 and epithelial growth factor （EGF） in Hp positive gastric cancer are higher than those in Hp negative gastric cancer. High level of EGF receptor （EGFR） binds to ligand of EGF or TGF and activates tyrosine kinase, thereby promotes tumor cells proliferation. Simultaneously, tumor cells secrete EGF and TGF and stimulate EGFR overexpression, forming a vicious circle. There is also emerging evidence that the two important angiogenic factors, vascular endothelial growth factor and midkine, are correlated with Hp infection. Hp infection was positively correlated with the activation of p-STAT3, thereby up-regulating the levels of Mcl-1, survivin, Bcl-2, Bcl-xL Cyclin D1 and VEGF and other target protein and regulating tumor cells proliferation and apoptosis.
