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Updated: Jul 23, 2026

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode
Published on: June 18, 2016
N-acetylcysteine, a novel treatment for Helicobacter pylori infection
Hien Quoc Huynh1, Richard T L Couper, Cuong D Tran
1Women's Children's Hospital, South Australia. hien.huynh@ualberta.ca
Abstract:
N-Acetylcysteine (NAC), being both a mucolytic agent and a thiol-containing antioxidant, may affect the establishment and maintenance of H. pylori infection within the gastric mucus layer and mucosa. Agar and broth dilution susceptibility tests determined the MIC of H. pylori strain SSI to NAC. H. pylori load in SSI strain-infected C57BL mice was determined as colony forming units per gram of gastric tissue. Gastritis assessment was scored and gastric surface hydrophobicity was determined by contact angle measurement. MICs of NAC were 5 to 10 and 10 to 15 mg/ml using the agar dilution and broth dilution methods, respectively. NAC (120 mg per day for 14 days) reduced the H. pylori load in mice by almost 1 log compared with sham treatment. Pretreatment with NAC (40 mg/day) also significantly reduced the H. pylori load but did not prevent H. pylori colonization. Both H. pylori infection and NAC reduced the surface hydrophobicity of murine gastric mucosa. No significant differences were observed in the gastritis scores of H. felis- or H. pylori-infected mice receiving either NAC or sham treatments. This study demonstrates that NAC inhibits the growth of H. pylori in both agar and broth susceptibility tests and in H. pylori-infected mice. NAC did not alter the severity of H. pylori- or H. felis-induced gastritis.
Insights
N-Acetylcysteine (NAC) inhibits Helicobacter pylori (H. pylori) growth in vitro and reduces bacterial load in mice. NAC treatment also decreased gastric surface hydrophobicity but did not affect gastritis severity.
Area of Science:
- Microbiology
- Gastroenterology
- Pharmacology
Background:
- Helicobacter pylori (H. pylori) infection is a major cause of gastritis and peptic ulcers.
- N-Acetylcysteine (NAC) possesses mucolytic and antioxidant properties, suggesting potential roles in modulating H. pylori infection.
- The impact of NAC on H. pylori colonization and associated gastric pathology requires investigation.
Purpose of the Study:
- To evaluate the in vitro and in vivo effects of N-Acetylcysteine (NAC) on Helicobacter pylori (H. pylori) growth and infection.
- To assess NAC's influence on H. pylori load, gastric mucosal hydrophobicity, and gastritis severity in a murine model.
Main Methods:
- Minimum Inhibitory Concentration (MIC) of NAC against H. pylori was determined using agar and broth dilution methods.
- H. pylori load was quantified in infected mice treated with NAC or sham.
- Gastric mucosal hydrophobicity and gastritis scores were assessed.
Main Results:
- NAC exhibited inhibitory activity against H. pylori, with MICs ranging from 5-15 mg/ml depending on the method.
- NAC administration (120 mg/day for 14 days) significantly reduced H. pylori load in mice by approximately 1 log.
- Both H. pylori infection and NAC treatment decreased gastric surface hydrophobicity; NAC did not alter gastritis scores.
Conclusions:
- N-Acetylcysteine demonstrates direct inhibitory effects on H. pylori growth in vitro and reduces bacterial burden in vivo.
- NAC may influence the gastric environment by altering mucosal hydrophobicity.
- NAC does not exacerbate H. pylori- or H. felis-induced gastritis in this model.
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