Antibiotic Resistance of Helicobacter pylori: Mechanisms and Clinical Implications

Abstract

Helicobacter pylori is a pathogenic bacterium associated with various gastrointestinal diseases, including chronic gastritis, peptic ulcers, mucosa-associated lymphoid tissue lymphoma, and gastric cancer. The increasing rates of H. pylori antibiotic resistance and the emergence of multidrug-resistant strains pose significant challenges to its treatment. This comprehensive review explores the mechanisms underlying the resistance of H. pylori to commonly used antibiotics and the clinical implications of antibiotic resistance. Additionally, potential strategies for overcoming antibiotic resistance are discussed. These approaches aim to improve the treatment outcomes of H. pylori infections while minimizing the development of antibiotic resistance. The continuous evolution of treatment perspectives and ongoing research in this field are crucial for effectively combating this challenging infection.

Keywords: Antibiotic Resistance; Antimicrobial Stewardship; Helicobacter pylori; Multidrug Resistance.

Fig. 1. Overview of molecular mechanism of antibiotic resistance in H. pylori and strategies to overcome this resistance. This image was created with BioRender.com.

FrxA = NAD(P)H flavin oxidoreductase, GI = gastrointestinal, GyrA = DNA gyrase subunit A, GyrB = DNA gyrase subunit B, PBP = penicillin-binding protein, PCAB = potassium-competitive acid blocker, RdxA = oxygen-insensitive NAD(P)H nitroreductase, RpoB = β-subunit of DNA-dependent RNA polymerase, rRNA = ribosomal RNA, tRNA = transfer RNA.