Conclusion:
IL-17 plays an important role in H. pylori-related gastritis and in the reduction of Helicobacter infection in mice following immunization. “
“Background: Small molecule library Lafutidine is an H2-receptor antagonist with gastroprotective action through capsaicin-sensitive afferent neurons and relatively inexpensive compare to proton-pump inhibitors (PPIs). A 7-day course of PPIs–amoxicillin–metronidazole is recommended as standard second-line Helicobacter pylori therapy and is covered by national health insurance in Japan. The aim of this study was to determine the efficacy and safety of second-line eradication using the H2-receptor antagonist lafutidine as a substitute for a PPI. Materials and Methods: Fifty-two patients who failed in first-line eradication using PPI–amoxicillin–clarithromycin were randomly assigned to a 7-day course of rabeprazole at 10 mg b.i.d., amoxicillin at 750 mg b.i.d., and metronidazole at 250 mg b.i.d. (RPZ-AM) or a 7-day course of lafutidine at 10 mg t.i.d., amoxicillin at 750 mg b.i.d., and metronidazole at 250 mg b.i.d. (LFT-AM) as second-line therapy. Eradication was assessed by the 13C urea breath test. A drug susceptibility test was performed before the second-line therapy. Results: Prior to second-line H. pylori eradication, the rate of resistance to clarithromycin was 86.5% and the rate of resistance
to metronidazole was 3.8%. The eradication rates Selleck 3-MA for both LFT-AM and RPZ-AM groups were 96% (95%CI = 88.6–100%). There were no severe adverse events in either group. Conclusions: Lafutidine plus metronidazole–amoxicillin as second-line therapy provided a high mafosfamide eradication rate and safe treatment similar to a PPI-based regimen. Lafutidine-based
eradication therapy is therefore considered to be a promising alternative and is also expected to reduce health care costs in H. pylori eradication. “
“Background: Helicobacter pylori infection can lead to the development of gastritis, peptic ulcers and gastric cancer, which makes this bacterium an important concern for human health. Despite evoking a strong immune response in the host, H. pylori persists, requiring complex antibiotic therapy for eradication. Here we have studied the impact of a patient’s immune serum on H. pylori in relation to macrophage uptake, phagosome maturation, and bacterial killing. Materials and Methods: Primary human macrophages were infected in vitro with both immune serum-treated and control H. pylori. The ability of primary human macrophages to kill H. pylori was characterized at various time points after infection. H. pylori phagosome maturation was analyzed by confocal immune fluorescence microscopy using markers specific for H. pylori, early endosomes (EEA1), late endosomes (CD63) and lysosomes (LAMP-1). Results: Immune serum enhanced H. pylori uptake into macrophages when compared to control bacteria.