The intersection of microbial food safety and antimicrobial resistance (AMR) represents a mounting global threat with profound implications for public health, food safety, and sustainable development. This review explores the complex pathways through which foodborne pathogens—such as Salmonella spp., Escherichia coli (E. coli), Listeria monocytogenes (L. monocytogenes), and Campylobacter spp.—acquire and disseminate resistance within human, animal, and environmental ecosystems. Emphasizing a One Health framework, we examine the drivers of AMR across sectors, including the misuse of antibiotics in agriculture, aquaculture, and clinical settings, and assess the role of environmental reservoirs in sustaining and amplifying resistance genes. We further discuss the evolution of surveillance systems, regulatory policies, and antimicrobial stewardship programs (ASPs) designed to mitigate resistance across the food chain. Innovations in next-generation sequencing, metagenomics, and targeted therapeutics such as bacteriophage therapy, antimicrobial peptides (AMPs), and CRISPR-based interventions offer promising alternatives to conventional antibiotics. However, the translation of these advances into practice remains uneven, particularly in low- and middle-income countries (LMICs) facing significant barriers to diagnostic access, laboratory capacity, and equitable treatment availability. Our analysis underscores the urgent need for integrated, cross-sectoral action—anchored in science, policy, and education—to curb the global spread of AMR. Strengthening surveillance, investing in research, promoting responsible antimicrobial use, and fostering global collaboration are essential to preserving the efficacy of existing treatments and ensuring the microbiological safety of food systems worldwide.

Helicobacter pylori (H. pylori) infection is one of the major causes of gastric cancer and remains an important global health concern. However, the biological processes linking chronic infection to malignant transformation are still not fully understood. Unlike previous reviews that mainly emphasized oxidative injury or individual virulence factors, this review synthesizes current evidence into an integrated redox-centered framework for gastric carcinogenesis. This framework links signaling pathways, epithelial adaptation, diagnostic interpretation, and therapeutic stratification. Current evidence indicates that persistent redox imbalance interacts with inflammatory signaling, mitochondrial dysfunction, metabolic reprogramming, epigenetic alteration, microbiome disruption, and oncogenic pathway activation throughout disease progression. Particular attention is given to the coordinated roles of NF-κB, STAT3, PI3K/AKT, HIF-1α, β-catenin, and Hippo-YAP signaling pathways. These pathways contribute to epithelial survival, chronic inflammation, genomic instability, and malignant transformation. This review additionally introduces a conceptual threshold model describing the progression from early epithelial stress to increasingly stable oncogenic reprogramming during long-standing infection. In addition, the limitations of conventional infection-centered diagnostics and non-selective antioxidant therapies are critically discussed. Emerging diagnostic approaches include oxidative injury biomarkers, transcriptomic and epigenetic profiling, artificial intelligence-assisted pathology, and multi-parameter predictive models. These approaches may improve risk stratification and facilitate earlier identification of high-risk gastric states. The translational implications further emphasize the importance of stage-specific and compartment-directed therapeutic strategies, particularly selective redox modulation and precision-guided targeting. Overall, this review provides a multidimensional perspective on H. pylori-associated gastric carcinogenesis and highlights future directions for predictive diagnostics, mechanistic stratification, and precision-based therapeutic development.

Acinetobacter baumannii (A. baumannii) is a major cause of multidrug-resistant infections, yet resistance is often interpreted from a gene-centered perspective that does not explain inconsistent treatment outcomes. This narrative review redefines resistance as a treatment-associated phenotype arising from interactions among molecular resistance mechanisms, bacterial physiology, and the infection environment. Unlike previous reviews that examine determinants in isolation, this work integrates efflux, permeability, enzymatic activity, and target modification with phenotypic states such as structured growth, metabolic adaptation, and stress response within a unified framework. Within this framework, bacterial elimination depends on whether antibiotics maintain sufficient target engagement under infection conditions. Antibiotic performance varies with local environment, population diversity, and cellular activity, which explains the gap between laboratory susceptibility results and clinical response. Antimicrobial failure therefore results from the combined effects of impaired drug exposure, adaptive bacterial physiology, and resistance mechanisms within the infection environment. Based on this framework, therapeutic strategies are reconsidered with emphasis on enhancing drug access, modulating cellular behavior, and disrupting population structures that sustain persistence. The review also highlights key gaps, including limited representation of infection environments in experimental models, insufficient resolution of population diversity, and weak integration between pharmacokinetics and bacterial physiology. This framework supports a mechanistic interpretation of resistance and therapeutic response in A. baumannii.

Drug-resistant biofilm infections remain a major challenge for medical devices and implants. Biofilm formation can reduce antimicrobial effectiveness through physiological heterogeneity, tolerance, persistence, and interactions with the host and biomaterial surface. Antimicrobial biomaterials have been developed to prevent colonization, detect infection, provide antimicrobial activity, control established biofilms, and support tissue recovery. However, their performance depends on the biological context in which they function. This review examines these strategies through interactions among the host, microbe, and material, using carbapenem-resistant Acinetobacter baumannii, methicillin-resistant Staphylococcus aureus, and carbapenem-resistant Pseudomonas aeruginosa as selected biological stress-test examples for evaluating biomaterial performance. It also considers the limitations in current evaluation, including planktonic testing, biological conditioning, microbial adaptation, effects on non-target microorganisms, material stability, manufacturing, and clinical translation. Antimicrobial activity alone does not establish effective performance in infection. Material function must match the microbial state, host environment, and intended clinical use while maintaining host compatibility and function during use. We propose infection resilience as a design framework organized around Prevent, Detect, Respond, Resolve, and Regenerate. Infection resilience refers to coordinated material performance under changing microbial and host conditions rather than the number of functions incorporated into a material. This framework offers a practical basis for more biologically relevant evaluation and purposeful design of antimicrobial biomaterials for drug-resistant biofilm infections.