Bacterial Stress Responses and Antibiotic Resistance Phenotypes

Dear Colleagues,

Bacteria employ exquisitely controlled stress response mechanisms to survive and adapt to a myriad of growth-compromising environmental insults, including cell envelope damage, nutrient deprivation, heavy metals, oxidative and nitrosative stress, and antimicrobial drug exposure. Growing research in this area continues to demonstrate a direct linkage between stress response systems and the development of antimicrobial resistance in bacteria. Stress response genes function as determinants of antibiotic resistance, and the induction of bacterial stress response systems plays important roles in the conversion of heterogeneous resistance phenotypes to high-level, homogeneous-resistance phenotypes. This interrelationship between stress and resistance is reinforced by evidence that the inactivation of stress response genes correlates with an increased susceptibility of bacteria to antibiotics. Additionally, random stress-induced mutations (adaptive mutagenesis) also affect antibiotic resistance in bacteria. Given that the global emergence of antibiotic resistance poses an increasing threat to the effective chemotherapeutic management of infectious diseases, the molecular components comprising adaptive cellular responses to stress are a potential valuable source of new targets for clinical intervention. This Special Issue of Antibiotics is seeking manuscript submissions that advance our understanding of the stress-related molecular determinants that contribute to the development of antibiotic resistance phenotypes in bacteria. Submissions providing insight into the mechanistic link between nutrient (stringent)/cell envelope/oxidative/nitrosative stress and antibiotic resistance in bacteria are particularly encouraged

Prof. Dr. Dorothea K. Thompson
Guest Editor

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