RESUMO
Survival strategies of human-associated microbes to drug exposure have been mainly studied in the context of bona fide pathogens exposed to antibiotics. Less well understood are the survival strategies of non-pathogenic microbes and host-associated commensal communities to the variety of drugs and xenobiotics to which humans are exposed. The lifestyle of microbial commensals within complex communities offers a variety of ways to adapt to different drug-induced stresses. Here, we review the responses and survival strategies employed by gut commensals when exposed to drugs-antibiotics and non-antibiotics-at the individual and community level. We also discuss the factors influencing the recovery and establishment of a new community structure following drug exposure. These survival strategies are key to the stability and resilience of the gut microbiome, ultimately influencing the overall health and well-being of the host.
Assuntos
Antibacterianos , Bactérias , Microbioma Gastrointestinal , Humanos , Microbioma Gastrointestinal/efeitos dos fármacos , Antibacterianos/farmacologia , Bactérias/efeitos dos fármacos , Xenobióticos/farmacologia , Simbiose , Trato Gastrointestinal/microbiologia , Trato Gastrointestinal/efeitos dos fármacos , Farmacorresistência Bacteriana , Interações entre Hospedeiro e Microrganismos/efeitos dos fármacosRESUMO
Abstract INTRODUCTION: Studies have demonstrated that pathogens react to the harsh conditions in human tissues by inducing mechanisms that promote survival. METHODS: Persistence and biofilm-forming ability were evaluated during stress conditions that mimic those in the host. RESULTS: Carbon-source availability had a positive effect on Staphylococcus epidermidis RP62A adhesion during hypoxia, accompanied by a decrease in pH. In contrast, iron limitation led to decreased surface-adherent biomass, accompanied by an increase medium acidification and lactate levels. Interestingly, iron starvation and hypoxia induced persister cells in planktonic culture. CONCLUSIONS: These findings highlight the role of host stress in the virulence of S. epidermidis.