Abstract
Antibiotic treatment failure of infection is common and frequently occurs in the absence of genetically encoded antibiotic resistance mechanisms. In such scenarios, the ability of bacteria to enter a phenotypic state that renders them tolerant to the killing activity of multiple antibiotic classes is thought to contribute to antibiotic failure. Phagocytic cells, which specialize in engulfing and destroying invading pathogens, may paradoxically contribute to antibiotic tolerance and treatment failure. Macrophages act as reservoirs for some pathogens and impede penetration of certain classes of antibiotics. In addition, increasing evidence suggests that subpopulations of bacteria can survive inside these cells and are coerced into an antibiotic-tolerant state by host cell activity. Uncovering the mechanisms that drive immune-mediated antibiotic tolerance may present novel strategies to improving antibiotic therapy.
Highlights
Bactericidal activity of antibiotics in vitro at low, physiologically achievable concentrations can rapidly kill bacteria in culture, and, if this cidality were realized in vivo, it could have a major impact on antibiotic treatment duration and efficacy
Immune cells evoke a plethora of stresses to eliminate invading pathogens, but there is mounting evidence that components of the innate immune response are antagonistic to antibiotics [5,6,7,9]
Interactions between the innate immune system and bacterial pathogens have definite impacts on antibiotic efficacy. This realization opens the door to using immunomodulators to maximize antibiotic efficacy to improve the treatment of infection
Summary
AAntUibi:oPticleatrseeactomnfeirnmt tfhaailtuarlelhoefaidnifnegclteivoenlsiasrceorempmresoenntaenddcofrereqcutleyn: tly occurs in the absence of genetically encoded antibiotic resistance mechanisms. In such scenarios, the ability of bacteria to enter a phenotypic state that renders them tolerant to the killing activity of multiple antibiotic classes is thought to contribute to antibiotic failure. Phagocytic cells, which specialize in engulfing and destroying invading pathogens, may paradoxically contribute to antibiotic tolerance and treatment failure. Macrophages act as reservoirs for some pathogens and impede penetration of certain classes of antibiotics. Increasing evidence suggests that subpopulations of bacteria can survive inside these cells and are coerced into an antibiotic-tolerant state by host cell activity. Uncovering the mechanisms that drive immune-mediated antibiotic tolerance may present novel strategies to improving antibiotic therapy
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