Publications by authors named "Rachel T Giorgio"

Antibiotic-recalcitrant infections, defined as the prolonged carriage of pathogenic bacteria even in the presence of antibiotics, are often caused by bacteria that are genetically susceptible to the drug. These recalcitrant bacteria fail to proliferate in the presence of antibiotics but remain viable such that they may recolonize their niche following antibiotic withdrawal. Significant progress has been made in our understanding of antibiotic-recalcitrant Salmonella, which are thought to be the source of infection relapse.

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The rise of antimicrobial failure is a global emergency, and causes beyond typical genetic resistance must be determined. One probable factor is the existence of subpopulations of transiently growth-arrested bacteria, persisters, that endure antibiotic treatment despite genetic susceptibility to the drug. The presence of persisters in infected hosts has been successfully established, notably through the development of fluorescent reporters.

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Transcription factors control gene expression; among these, transcriptional repressors must liberate the promoter for derepression to occur. Toxin-antitoxin (TA) modules are bacterial elements that autoregulate their transcription by binding the promoter in a T:A ratio-dependent manner, known as conditional cooperativity. The molecular basis of how excess toxin triggers derepression has remained elusive, largely because monitoring the rearrangement of promoter-repressor complexes, which underpin derepression, is challenging.

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Article Synopsis
  • The host environment significantly affects how effective antibiotics are, especially during infections caused by resistant bacteria known as persisters.
  • These persisters can temporarily evade the effects of antibiotics, contributing to treatment failures and recurrent infections.
  • Recent research found that reactive nitrogen species (RNS) in the host not only protect persisters from certain antibiotics but also make them more vulnerable to others, like fluoroquinolones, by disrupting their ability to expel these drugs.
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Genetically susceptible bacteria can escape the action of bactericidal antibiotics through antibiotic tolerance or persistence. However, one major difference between the two phenomena is their distinct penetrance within an isogenic population. While with antibiotic persistence, susceptible and persister cells co-exist, antibiotic tolerance affects the entire bacterial population.

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The microbial cell surface is a site of critical microbe-host interactions that often control infection outcomes. Defining the set of host proteins present at this interface has been challenging. Here we used a surface-biotinylation approach coupled to quantitative mass spectrometry to identify and quantify both bacterial and host proteins present on the surface of diarrheal fluid-derived Vibrio cholerae in an infant rabbit model of cholera.

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Toxin-antitoxin (TA) systems are a large family of genes implicated in the regulation of bacterial growth and its arrest in response to attacks. These systems encode nonsecreted toxins and antitoxins that specifically pair, even when present in several paralogous copies per genome. Salmonella enterica serovar Typhimurium contains three paralogous TacAT systems that block bacterial translation.

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The function of , a bacterial gene predicted to encode an inner membrane protein, is largely unknown. Early studies in linked to Colicin V secretion and recent work revealed that it is required for robust intestinal colonization by diverse enteric pathogens. In enterohemorrhagic (EHEC), is required for resistance to the bile salt deoxycholate (DOC).

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Despite the advent of new techniques for genetic engineering of bacteria, allelic exchange through homologous recombination remains an important tool for genetic analysis. Currently, -based vector systems are often used for allelic exchange, but counterselection escape, which prevents isolation of cells with the desired mutation, occasionally limits their utility. To circumvent this, we engineered a series of "pTOX" allelic-exchange vectors.

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Introduction: Preeclampsia represents a major public health burden worldwide, but predictive and diagnostic biomarkers are lacking. Metabolomics is emerging as a valuable approach to generating novel biomarkers whilst increasing the mechanistic understanding of this complex condition.

Objectives: To summarize the published literature on the use of metabolomics as a tool to study preeclampsia.

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