RESUMO
Helicobacter pylori is a gastric pathogen that colonizes approximately 50% of the world's population. Infection with H. pylori causes chronic inflammation and significantly increases the risk of developing duodenal and gastric ulcer disease and gastric cancer. In the present study, we found that phenyl lactic acid (PLA) derived from Lactobacillus plantarum ZJ316 (L. plantarum ZJ316) can directly inhibit the growth and urease activity of H. pylori in vitro with a minimum inhibitory concentration (MIC) of 2.5 mg mL-1. Moreover, PLA also caused a dramatic morphological transformation from a spiral to a coccoid form in H. pylori. In this work, we also analyzed the beneficial effects of PLA in mice. The results showed that PLA administration ameliorated H. pylori-induced gastric mucosal damage and significantly decreased lymphocyte infiltration and inflammatory cytokines, including interleukin-1ß (IL-1ß), interleukin 6 (IL-6), and interferon-γ (IFN-γ) by 59.93%, 63.95%, and 48.05%, respectively, but elevated the interleukin-10 (IL-10) and glutathione (GSH) levels. Furthermore, PLA administration improved microbiota diversity with increased Bacteroidetes abundance and decreased Proteobacteria abundance by 46.39% and 24.05%, respectively. PLA also significantly reduced the abundance of H. pylori but increased the relative abundances of potential beneficial bacteria, such as Faecalibacterium, Bifidobacterium, and Lactobacillus. These results demonstrated that PLA can ameliorate H. pylori-induced inflammation and support beneficial gut bacteria, providing a new perspective against H. pylori infection.
Assuntos
Infecções por Helicobacter , Helicobacter pylori , Camundongos , Animais , Infecções por Helicobacter/tratamento farmacológico , Infecções por Helicobacter/microbiologia , Camundongos Endogâmicos C57BL , Mucosa Gástrica , Inflamação , Ácido Láctico , PoliésteresRESUMO
Alzheimer's disease (AD) is the most common neurodegenerative disease. More and more evidence show that DNA methylation is closely related to the pathological mechanism of AD. Many AD-associated differentially methylated genes, regions and CpG sites have been identified in recent researches, which may have great potential in clinical research. However, there is no dedicated database to collect AD-related differential methylation up to now. To provide a reference to researchers, we design a database named ADmeth by manually curating relevant articles, which contains a total of 16,709 AD-related differentially methylated items identified from different brain regions and different cell types in the blood, involving 209 genes, 2,229 regions and 14,271 CpG sites. The ADmeth database provides user-friendly pages to search, submit and download data. We hope that the ADmeth database can facilitate researchers to select candidate AD-associated methylation markers in revealing the pathological mechanism of AD and promote the cell-free DNA based non-invasive diagnosis of AD. The ADmeth database is available at http://www.biobdlab.cn/ADmeth.