The burgeoning field of pharmacomicrobiomics offers promising insights into the intricate interplay between the microbiome and cancer, shaping responses to diverse treatment modalities. This review aims to analyze the molecular mechanisms underlying interactions between distinct microbiota types and cancer, as well as their influence on treatment outcomes. We explore how the microbiome impacts antitumor immunity, and response to chemotherapy, immunotherapy, and radiation therapy, unveiling its multifaceted roles in cancer progression and therapy resistance.
View Article and Find Full Text PDFstands out as a major opportunistic pathogen responsible for both hospital- and community-acquired bacterial infections. This study comprehensively assesses the antibiotic resistance, amikacin persistent patterns, and biofilm-forming ability of 247 isolates of obtained from an intensive care unit of a tertiary hospital in Vietnam. Microdilution assays, conducted on a 96-well plate, determined the minimum inhibitory concentrations (MICs) of amikacin.
View Article and Find Full Text PDFPersisters are transiently nongrowing and antibiotic-tolerant phenotypic variants identified in major human pathogens, including intracellular Staphylococcus aureus. Due to their capacity to regrow once the environmental stress is relieved and to promote resistance, persisters possibly contribute to therapeutic failures. While persistence and its related quiescence have been mostly studied under starvation, little is known within host cell environments.
View Article and Find Full Text PDFResistance is notoriously high in Asia but may not entirely explain therapeutic failures. Specific modes of bacterial life, such as biofilm or intracellular survival, may also contribute to the persistent and/or recurrent character of infections. Most isolates form biofilm and many survive and even thrive intracellularly.
View Article and Find Full Text PDFInt J Antimicrob Agents
September 2017
Clostridium difficile T10 and Clostridium bolteae 90B3 were co-resistant to phenicols, lincosamides, oxazolidinones, pleuromutilins and streptogramin A (PhLOPS) and harbored an unreported cfr-like determinant that may alter the 23S rRNA by mA2503 methylation. The cfr-like cfr(C) gene was cloned in C. difficile 630Δerm in which it conferred PhLOPS resistance.
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