Amanda Brady

ORCID: 0000-0002-4869-6209
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About
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Research Areas
  • Yersinia bacterium, plague, ectoparasites research
  • Plant-based Medicinal Research
  • Oral microbiology and periodontitis research
  • Ethnobotanical and Medicinal Plants Studies
  • Pneumonia and Respiratory Infections
  • Insect and Pesticide Research
  • Pharmacological Effects of Natural Compounds
  • Bee Products Chemical Analysis
  • Neonatal and Maternal Infections
  • Vibrio bacteria research studies
  • Bacillus and Francisella bacterial research
  • Essential Oils and Antimicrobial Activity
  • Bacterial Identification and Susceptibility Testing
  • Vector-borne infectious diseases

University of Colorado Anschutz Medical Campus
2024-2025

University of Louisville
2021-2024

University of Louisville Hospital
2024

Subverting the host immune response to inhibit inflammation is a key virulence strategy of Yersinia pestis . The inflammatory cascade tightly controlled via sequential action lipid and protein mediators inflammation. Because delayed essential for Y cause lethal infection, defining mechanisms manipulate necessary understand this pathogen’s virulence. While previous studies have established that actively inhibits expression proteins mediate inflammation, there currently gap in our...

10.1371/journal.ppat.1011280 article EN cc-by PLoS Pathogens 2024-01-25

ABSTRACT Group B Streptococcus (GBS) is a Gram-positive pathobiont that commonly colonizes the gastrointestinal and lower female genital tracts but can cause sepsis pneumonia in newborns leading of neonatal meningitis. Despite resulting disease severity, pathogenesis GBS not completely understood, especially during early phases infection. To investigate factors necessary for bloodstream survival, we performed transposon (Tn) mutant screen our bacteremia infection model using mariner library...

10.1128/iai.00540-24 article EN cc-by Infection and Immunity 2025-02-26

Significance Transition metals are required for proper cellular function, which renders them critical all life. To restrict bacterial infection, eukaryotic organisms actively sequester these transition metals, a concept referred to as nutritional immunity. Consequently, pathogens have evolved dedicated mechanisms acquire in order colonize the host. During human plague, Yersinia pestis overcomes iron limitation via production of secreted siderophore yersiniabactin. Here, we identify an...

10.1073/pnas.2104073118 article EN Proceedings of the National Academy of Sciences 2021-10-29

Fleas transmit Yersinia pestis directly within the dermis of mammals to cause bubonic plague. Syringe-mediated inoculation is widely used recapitulate plague and study Y. pathogenesis. However, intradermal needle tedious, error prone, poses a significant safety risk for laboratorians. Microneedle arrays (MNAs) are micron-scale polymeric structures that deliver materials dermis, while minimizing sticks. We demonstrated MNA viable strategy bacterial virulence by defining parameters needed...

10.1016/j.isci.2023.108600 article EN cc-by-nc-nd iScience 2023-11-30

Abstract Leukotriene B4 (LTB 4 ) is critical for initiating the inflammatory cascade in response to infection. However, Yersinia pestis colonizes host by inhibiting timely synthesis of LTB and inflammation. Here, we show that bacterial type 3 secretion system (T3SS) primary pathogen associated molecular pattern (PAMP) responsible production leukocytes Salmonella , but inhibited Yop effectors during interactions. Moreover, unexpectedly discovered T3SS-mediated neutrophils macrophages require...

10.1101/2024.07.01.601466 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-07-02

Abstract Group B Streptococcus (GBS) is a Gram-positive pathobiont that commonly colonizes the gastrointestinal and lower female genital tracts but can cause sepsis pneumonia in newborns leading of neonatal meningitis. Despite resulting disease severity, pathogenesis GBS not completely understood, especially during early phases infection. To investigate factors necessary for blood stream survival, we performed transposon (Tn) mutant screen our bacteremia infection model using mariner library...

10.1101/2024.07.30.605887 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-07-30

Leukotriene B4 (LTB 4 ) is an inflammatory lipid produced in response to pathogens that critical for initiating the cascade needed control infection. However, during plague, Yersinia pestis inhibits timely synthesis of LTB and subsequent inflammation. Using bacterial mutants, we previously determined Y . via action Yop effector proteins are directly secreted into host cells through a type 3 secretion system (T3SS). Here, show T3SS primary pathogen associated molecular pattern (PAMP) required...

10.1371/journal.ppat.1012651 article EN cc-by PLoS Pathogens 2024-10-18

is the etiological agent of human plague. However, certain evolutionarily divergent subspecies have different host specificities and virulence capacity compared to more commonly studied strains with pandemic potential. This resource examines 10 diverse isolates representing some most understudied referred as

10.1128/mra.00996-24 article EN Microbiology Resource Announcements 2024-12-10

is the gram-negative, facultative intracellular bacterium that causes disease known as plague. Due to risk for aerosol transmission, a low infectious dose, and acute lethal nature of pneumonic plague, research activities with

10.1089/apb.2023.0022 article EN Applied Biosafety 2024-04-10

Abstract Subverting the host immune response to inhibit inflammation is a key virulence factor of Yersinia pestis . The inflammatory cascade tightly controlled via sequential action lipid and protein mediators inflammation. Because delayed essential for Y. cause lethal infection, defining mechanisms used by manipulate necessary understand this pathogen’s virulence. While previous studies have established that actively inhibits expression proteins mediate inflammation, there currently gap in...

10.1101/2023.03.13.532349 preprint EN cc-by bioRxiv (Cold Spring Harbor Laboratory) 2023-03-13
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