Kara R. Eichelberger

ORCID: 0000-0003-4532-9486
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About
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Research Areas
  • Yersinia bacterium, plague, ectoparasites research
  • Antimicrobial Resistance in Staphylococcus
  • Antifungal resistance and susceptibility
  • Orthopedic Infections and Treatments
  • Bacterial biofilms and quorum sensing
  • Plant-based Medicinal Research
  • Pharmacological Effects of Natural Compounds
  • Vector-borne infectious diseases
  • Vibrio bacteria research studies
  • Infective Endocarditis Diagnosis and Management
  • Bacillus and Francisella bacterial research
  • Bone Metabolism and Diseases
  • Oral microbiology and periodontitis research
  • Streptococcal Infections and Treatments
  • Osteomyelitis and Bone Disorders Research
  • Biomarkers in Disease Mechanisms
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Legionella and Acanthamoeba research
  • Monoclonal and Polyclonal Antibodies Research
  • Bone health and treatments
  • Gut microbiota and health
  • Probiotics and Fermented Foods
  • Escherichia coli research studies
  • Bacterial Infections and Vaccines

Vanderbilt University Medical Center
2021-2024

Vanderbilt University
2022

University of North Carolina at Chapel Hill
2015-2020

University of Pennsylvania
2013

Candida albicans and Staphylococcus aureus are two commonly associated pathogens that cause nosocomial infections with high morbidity mortality. Our prior current work using a murine model of polymicrobial intra-abdominal infection (IAI) demonstrates synergistic lethality is driven by Candida-induced upregulation functional S. α-toxin leading to sepsis organ damage. In order determine the candidal effector(s) mediating enhanced virulence, an unbiased screen C. transcription factor mutants...

10.1038/s41467-024-50058-w article EN cc-by Nature Communications 2024-07-09

ABSTRACT During pneumonic plague, the bacterium Yersinia pestis elicits development of inflammatory lung lesions that continue to expand throughout infection. This lesion and persistence are poorly understood. Here, we examine spatially distinct regions using laser capture microdissection transcriptome sequencing (RNA-seq) analysis identify transcriptional differences between microenvironments. We show cellular pathways involved in leukocyte migration apoptosis downregulated center compared...

10.1128/mbio.01530-15 article EN cc-by-nc-sa mBio 2015-10-14

Pneumonic plague is the most rapid and lethal form of Yersinia pestis infection. Increasing evidence suggests that Y. employs multiple levels innate immune evasion and/or suppression to produce an early "pre-inflammatory" phase pulmonary infection, after which disease highly inflammatory in lung 100% fatal. In this study, we show IL-1β/IL-18 cytokine activation occurs bacteria enter lung, eventually contributes inflammation pathology during later stages However, effects IL-1β/IL-1-receptor...

10.1371/journal.ppat.1004688 article EN cc-by PLoS Pathogens 2015-03-17

Summary The lipopolysaccharide ( LPS ) of H . influenzae is highly variable. Much the structural diversity derived from phase variation, or high frequency on‐off switching, molecules attached during biosynthesis. In this study, we examined dynamics variation following exposure to human serum as a source antibody and complement in multiple isolates. We show that lic2A , lgtC lex2A switch phase‐off phase‐on serial passage serum. These genes, which control attachment galα1–4gal di‐galactoside...

10.1111/mmi.12214 article EN Molecular Microbiology 2013-04-12

Yersinia pestis is the causative agent of plague and one deadliest human pathogens. The pneumonic form Y. infection has played a critical role in severity both historical modern outbreaks, yet host-pathogen interactions that govern lethality pulmonary infections are incompletely understood. Here, we report inhibits neutrophil degranulation during infection, rendering neutrophils ineffective allowing unrestricted growth lungs. This coordinated inhibition granule release not only demonstrates...

10.1128/mbio.02759-19 article EN cc-by mBio 2019-12-09

Inflammatory bowel disease (IBD) is characterized by severe gastrointestinal inflammation, but many patients experience extra-intestinal disease. Bone loss one common manifestation of IBD that occurs through dysregulated interactions between osteoclasts and osteoblasts. Systemic inflammation has been postulated to contribute bone loss, the specific pathologic mechanisms have not yet fully elucidated. We hypothesized intestinal leads increased abundance altered function osteoclast progenitors.

10.1016/j.jcmgh.2022.07.002 article EN cc-by-nc-nd Cellular and Molecular Gastroenterology and Hepatology 2022-01-01

ABSTRACT Candida albicans and Staphylococcus aureus are two commonly associated pathogens that cause nosocomial infections with high morbidity mortality. Our prior current work using a murine model of polymicrobial intra-abdominal infection (IAI) uncovered synergistic lethality was driven by -induced upregulation functional S. ⍺-toxin leading to sepsis organ damage. In order determine the candidal effector(s) mediating enhanced virulence, an unbiased screen C. transcription factor mutants...

10.1101/2024.02.15.580531 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-02-15

Following inhalation, Yersinia pestis rapidly colonizes the lung to establish infection during primary pneumonic plague. Although several adhesins have been identified in spp., factors mediating early Y. adherence remain unknown. To identify genes important for plague, we used transposon insertion sequencing (Tn-seq). Wild-type and capsule mutant (Δcaf1) libraries were serially passaged vivo enrich nonadherent mutants using a mouse model of Sequencing revealed six that significantly enriched...

10.1128/msphere.00715-20 article EN cc-by mSphere 2020-08-04

Yersinia pestis is a highly virulent pathogen and the causative agent of bubonic, septicemic, pneumonic plague. Primary plague caused by inhalation respiratory droplets contaminated with Y. nearly 100% lethal within 4 to 7 days without antibiotic intervention.

10.1128/iai.00673-20 article EN cc-by Infection and Immunity 2020-12-01

Osteomyelitis can result from the direct inoculation of pathogens into bone during injury or surgery spread via bloodstream, a condition called hematogenous osteomyelitis (HOM). HOM disproportionally affects children, and more than half cases are caused by Staphylococcus aureus .

10.1128/iai.00180-21 article EN Infection and Immunity 2021-06-07

Abstract Background Staphylococcus aureus is a leading cause of antibiotic-resistant bacterial infections and can infect nearly every organ the human body. One common manifestation S. disease invasive bone infection, or osteomyelitis. Osteomyelitis one most difficult to treat infections, often necessitating prolonged antibiotic treatment surgical interventions. Hyperglycemia, elevated blood glucose concentration, increases risk for developing We hypothesized that adapts specifically altered...

10.1093/ofid/ofac492.156 article EN cc-by Open Forum Infectious Diseases 2022-12-01

Abstract Staphylococcus aureus is the major causative agent of bacterial osteomyelitis, an invasive infection bone. Osteomyelitis associated with significant bone destruction, bone-resorbing osteoclasts have been implicated in this process. Osteoclasts differentiate from monocyte precursors response to canonical osteoclastogenic cytokine RANKL, or receptor activator (NF)-κB ligand. The process osteoclastogenesis involves transcriptional reprogramming, thereby altering inflammatory responses...

10.4049/jimmunol.208.supp.164.12 article EN The Journal of Immunology 2022-05-01

Abstract Osteomyelitis can result from the direct inoculation of pathogens into bone during injury or surgery, spread via bloodstream, a condition called hematogenous osteomyelitis (HOM). HOM disproportionally affects children, and more than half cases are caused by Staphylococcus (S.) aureus . Laboratory models mostly utilize injection bacteria implantation foreign material, therefore do not directly interrogate pathogenesis pediatric osteomyelitis. In this study, we inoculated mice...

10.1101/2021.03.22.436444 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2021-03-22
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