title: The antibacterial mode of action of allitridi for its potential use as a therapeutic agent against Helicobacter pylori infection.
abstract: Eradication of Helicobacter pylori with traditional therapy often fails in clinical treatment. As a result, a novel efficacious therapeutic agent is strongly needed. Allitridi, a proprietary garlic derivative, has been successfully used to treat both systemic fungal and bacterial infections in China. Our previous study has shown a dose-dependent inhibitory effect of allitridi on H. pylori growth. However, the antibacterial mode of action of allitridi is still unclear. Proteomic analysis was used to study the global protein alterations induced by allitridi. A total of 21 protein spots were identified to be differentially expressed. Our results indicated that the bacteriostatic mechanism of allitridi in H. pylori can be attributed to its multitarget inhibitory effects in energy metabolism and biosynthesis including amino acid biosynthesis, protein synthesis, mRNA synthesis and fatty acid biosynthesis. Allitridi can also disturb the expression of antioxidant proteins and decrease the production of virulence factors. Western blot analysis showed that allitridi at subinhibitory concentrations can potently suppress the production of CagA and VacA. Our investigations on the antibacterial mode of action of allitridi provide an insight into the potential use of allitridi as a therapeutic agent against H. pylori infection.
authors.affiliation: Department of Microbiology and Key Laboratory for Experimental Teratology of Chinese Ministry of Education, School of Medicine, Shandong University, Jinan, Shandong, China.
authors.forename: Shuang
authors.initials: S
authors.lastname: Liu
authors.forename: Yundong
authors.initials: Y
authors.lastname: Sun
authors.forename: Wenjuan
authors.initials: W
authors.lastname: Li
authors.forename: Han
authors.initials: H
authors.lastname: Yu
authors.forename: Xi
authors.initials: X
authors.lastname: Li
authors.forename: Zhifang
authors.initials: Z
authors.lastname: Liu
authors.forename: Jiping
authors.initials: J
authors.lastname: Zeng
authors.forename: Yabin
authors.initials: Y
authors.lastname: Zhou
authors.forename: Chunyan
authors.initials: C
authors.lastname: Chen
authors.forename: Jihui
authors.initials: J
authors.lastname: Jia
mesh_terms: D000498:Allyl Compounds / Q000494:pharmacology* / Q000627:therapeutic use; D000900:Anti-Bacterial Agents / Q000494:pharmacology* / Q000627:therapeutic use; D000942:Antigens, Bacterial; D001426:Bacterial Proteins / Q000032:analysis / Q000037:antagonists & inhibitors; D053898:Biosynthetic Pathways / Q000187:drug effects; D002681:China; D015180:Electrophoresis, Gel, Two-Dimensional; D004734:Energy Metabolism / Q000187:drug effects; D016481:Helicobacter Infections / Q000188:drug therapy*; D016480:Helicobacter pylori / Q000737:chemistry / Q000187:drug effects*; D006801:Humans; D014176:Protein Biosynthesis / Q000187:drug effects; D020543:Proteome / Q000032:analysis; D013440:Sulfides / Q000494:pharmacology* / Q000627:therapeutic use; D037521:Virulence Factors / Q000037:antagonists & inhibitors
chemical_list: D000498:Allyl Compounds; D000900:Anti-Bacterial Agents; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D020543:Proteome; D013440:Sulfides; C074689:VacA protein, Helicobacter pylori; D037521:Virulence Factors; C080866:cagA protein, Helicobacter pylori; C042577:diallyl trisulfide