ABSTRACT
In a world where the emergence of resistant bacteria threatens the future use of many antibiotics, it is now critical to prescribe antibiotics carefully in order to minimize selective pressure. Limiting treatment duration would be one of the strategies to achieve this goal. Recent studies state that a reduction of the course of treatment is showing great benefit with no outcome difference.
Dans un contexte où les antibiotiques sont menacés par l'émergence de résistances bactériennes, il semble essentiel de développer des mesures pour une meilleure gestion de ces derniers, ce qui se résume par le concept d'antibiotic stewardship. Un des moyens de parvenir à cet objectif est la réduction de la durée de l'antibiothérapie. A cet effet, des études récentes ont énoncé des arguments en faveur de durées réduites de traitement.
Subject(s)
Anti-Bacterial Agents , Anti-Bacterial Agents/administration & dosage , Drug Administration Schedule , Drug Resistance, BacterialABSTRACT
Development of ectodermal appendages, such as hair, teeth, sweat glands, sebaceous glands, and mammary glands, requires the action of the TNF family ligand ectodysplasin A (EDA). Mutations of the X-linked EDA gene cause reduction or absence of many ectodermal appendages and have been identified as a cause of ectodermal dysplasia in humans, mice, dogs, and cattle. We have generated blocking antibodies, raised in Eda-deficient mice, against the conserved, receptor-binding domain of EDA. These antibodies recognize epitopes overlapping the receptor-binding site and prevent EDA from binding and activating EDAR at close to stoichiometric ratios in in vitro binding and activity assays. The antibodies block EDA1 and EDA2 of both mammalian and avian origin and, in vivo, suppress the ability of recombinant Fc-EDA1 to rescue ectodermal dysplasia in Eda-deficient Tabby mice. Moreover, administration of EDA blocking antibodies to pregnant wild type mice induced in developing wild type fetuses a marked and permanent ectodermal dysplasia. These function-blocking anti-EDA antibodies with wide cross-species reactivity will enable study of the developmental and postdevelopmental roles of EDA in a variety of organisms and open the route to therapeutic intervention in conditions in which EDA may be implicated.
