# Host-Pathogen Interactions in Staphylococcus aureus Infection (pp  312-313)

> **NIH NIH P41** · VANDERBILT UNIVERSITY · 2020 · $285,012

## Abstract

Bacterial pathogens are rapidly gaining resistance to antimicrobial therapeutics undermining
the ability of modern medicine to treat such infections [1,2]. The Centers for Disease Control and Prevention
reported over 2 million people in the United States become infected with drug-resistant bacteria annually,
causing at least 23,000 deaths [3]. In light of such reports, the need to identify and study novel targets for
antimicrobial intervention using emerging analytical technologies is paramount for the future successful
treatment of infectious diseases. One potential target for antimicrobial therapeutics involves transition metal
homeostasis at the pathogen-host interface [4,5]. Metals are an essential component of biological function for
all cells. It is estimated that 30-45% of all enzymes utilize a transition metal cofactor to enhance catalysis and
reactivity [6,7]. Therefore, bacterial pathogens proliferating within a host must obtain metals to survive and
grow, causing disease. In response, hosts seek to sequester these elements from pathogens, a process
known as nutritional immunity [4,8]. With a more detailed understanding of host mechanisms of metal
sequestration and bacterial mechanisms of metal scavenging, novel therapeutic targets can be discovered.
S. aureus is a Gram-positive pathogen that commensally colonizes the anterior nares of an estimated 25%
of the human population [9]. To cause disease, S. aureus breaches the initial site of infection and enters the
bloodstream where it can cause infectious lesions on virtually any organ [10]. A hallmark of these purulent
infectious foci, called abscesses, is the recruitment of host immune cells, including neutrophils and
macrophages, which generate oxidative stress in an attempt to kill the pathogen [11,12]. Abscess formation
has been studied extensively using histologically methods [10,13,14]; however, a molecular understanding of
organ-specific heterogeneity of bacterial virulence factor expression and host response is not yet understood.

## Key facts

- **NIH application ID:** 9842540
- **Project number:** 5P41GM103391-10
- **Recipient organization:** VANDERBILT UNIVERSITY
- **Principal Investigator:** RICHARD M CAPRIOLI
- **Activity code:** P41 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $285,012
- **Award type:** 5
- **Project period:** — → 2021-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9842540

## Citation

> US National Institutes of Health, RePORTER application 9842540, Host-Pathogen Interactions in Staphylococcus aureus Infection (pp  312-313) (5P41GM103391-10). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9842540. Licensed CC0.

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