# Investigating the role of Staphylococcus aureus strain-level diversity on neutrophil recruitment and wound healing in a cutaneous leishmaniasis infection

> **NIH NIH F31** · UNIVERSITY OF PENNSYLVANIA · 2021 · $46,036

## Abstract

PROJECT SUMMARY
 Cutaneous leishmaniasis is a parasitic infection that causes a variable spectrum of disease ranging from
single, self-healing lesions to disfiguring chronic lesions that do not heal despite treatment. While the factors
driving lesion chronicity are not clear, it is evident that many of the most severe forms of the disease are caused
by uncontrolled inflammation rather than high parasite burden. In mice, chronic leishmaniasis lesions are
characterized by increased neutrophil accumulation, persistent activation of inflammatory cytokines, and
increased infiltration of immune cells to the lesion site, all of which exacerbate tissue damage and delay healing.
Our lab has previously shown that colonizing microbes on the skin contribute to immunopathology in murine
models, however the role of the skin microbiota in regulating lesion healing is not known. We have found that
the most common bacteria colonizing human cutaneous leishmania lesions is Staphylococcus aureus (S.
aureus) which delays wound healing in a strain-specific manner across many different pathologies and is a potent
neutrophil recruiter. We have also been able to show that S. aureus clinical isolates cultured from human
cutaneous leishmaniasis lesions induce secretion of different amounts of neutrophil chemotactic factors such as
interleukin-8 (IL-8) by epithelial cells in a wound setting. Therefore, the central hypothesis of my proposal is that
S. aureus delays cutaneous leishmaniasis lesion healing through strain-variable neutrophil recruitment and
accumulation. In Aim 1, I will determine the strain-specific effect of S. aureus-mediated neutrophil recruitment
on wound healing and immunopathology in both a wounding model and in a cutaneous leishmaniasis model
using LysM-EGFP mice. In Aim 2, I will identify differences S. aureus neutrophil recruitment and persistence
genes across clinical isolates using whole genome sequencing and comparative genomics and associate this
data with clinical outcomes and RNA sequencing gene expression from human cutaneous leishmaniasis lesions.
These findings will collectively drive understanding of the strain-specific effects of S. aureus infection and
neutrophil recruitment on wound healing, uncover biomarkers that can be used to predict patient outcome, and
identify novel therapeutic targets in the treatment of cutaneous leishmaniasis.

## Key facts

- **NIH application ID:** 10313240
- **Project number:** 1F31AR079901-01
- **Recipient organization:** UNIVERSITY OF PENNSYLVANIA
- **Principal Investigator:** Victoria Lovins
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $46,036
- **Award type:** 1
- **Project period:** 2021-07-01 → 2024-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10313240

## Citation

> US National Institutes of Health, RePORTER application 10313240, Investigating the role of Staphylococcus aureus strain-level diversity on neutrophil recruitment and wound healing in a cutaneous leishmaniasis infection (1F31AR079901-01). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10313240. Licensed CC0.

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