Abstract Helicobacter pylori is a significant pathogen associated with a range of diseases, most notably gastritis and gastric cancer, making it a critical target for medical intervention. β-lactam antibiotics, known for their potent bactericidal properties, play a central role in clinical regimens aimed at eradicating H pylori. However, the increasing resistance of H pylori to β-lactams, compounded by the rise of multidrug-resistant strains, presents a major challenge to effective treatment. The molecular mechanisms underlying β-lactam resistance in H pylori are multifactorial, including (1) mutations in penicillin-binding proteins, (2) production of β-lactamases, (3) alterations in outer membrane permeability, and (4) activation of efflux pumps. These mechanisms not only reduce the efficacy of β-lactam antibiotics but also contribute to the emergence of multidrug-resistant H pylori strains. Understanding these molecular pathways is essential for the development of novel therapeutic strategies to overcome resistance and enhance the effectiveness of treatment for H pylori infections.
Zhou et al. (Thu,) studied this question.