Publications by authors named "A M PERAULT"
Article Synopsis
- Severe COVID-19 patients frequently experience coinfections with bacterial and fungal pathogens, leading to higher mortality rates compared to infections with just one pathogen.
- A study investigated blood and respiratory samples from hospitalized patients to analyze the relationship between SARS-CoV-2 and coinfections, finding no specific lineage associated with COVID-19 but noting trends in the virulence of bloodstream strains.
- Research using a mouse model demonstrated that SARS-CoV-2 infection increases susceptibility to subsequent infections with low-cytotoxicity pathogens, highlighting the enhanced risk of severe outcomes from these coinfections.
Depletion of microbiota increases susceptibility to gastrointestinal colonization and subsequent infection by opportunistic pathogens such as methicillin-resistant (MRSA). How the absence of gut microbiota impacts the evolution of MRSA is unknown. The present report used germ-free mice to investigate the evolutionary dynamics of MRSA in the absence of gut microbiota.
View Article and Find Full Text PDFThe quorum-sensing system links metabolism to virulence, in part by increasing bacterial survival during exposure to lethal concentrations of HO, a crucial host defense against . We now report that protection by surprisingly extends beyond post-exponential growth to the exit from stationary phase when the system is no longer turned on. Thus, can be considered a constitutive protective factor.
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- The quorum-sensing system enhances bacterial survival against the host's reactive oxygen species (ROS) by providing a protective factor that persists beyond typical metabolic stages when this system is usually active.
- Deletion of a specific gene led to increased respiration and fermentation in bacteria, but surprisingly resulted in lower ATP levels and growth due to a hyperactive metabolic state, making these mutant cells more vulnerable to oxidative damage.
- The study shows that the protective effects of quorum sensing not only help bacteria resist immune attacks but also influence the spread of infection in mice, indicating that this mechanism is likely a common defense strategy for various bacterial species.
Nosocomial infections caused by multidrug-resistant (MDR) Enterobacter cloacae complex (ECC) pathogens are on the rise. However, the virulence strategies employed by these pathogens remain elusive. Here, we study the interaction of ECC clinical isolates with human serum to define how this pathogen evades the antimicrobial action of complement, one of the first lines of host-mediated immune defense.
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