# Lactoferrin bridges antimicrobial and healing responses in Staphylococcus aureus skin infections

## TL;DR

Lactoferrin shows promise in treating Staphylococcus aureus skin infections by combining antimicrobial effects with wound healing properties.

## Contribution

This mini-review highlights lactoferrin's dual role in combating S. aureus infections through antimicrobial and tissue repair mechanisms.

## Key findings

- Lactoferrin inhibits S. aureus growth via iron sequestration and membrane disruption.
- It modulates inflammation, reduces oxidative stress, and promotes wound healing.
- Lactoferrin formulations enhance antibacterial activity when combined with antibiotics or bacteriophages.

## Abstract

Staphylococcus aureus is a leading cause of skin and wound infections worldwide, with methicillin-resistant strains (MRSA) posing a persistent clinical challenge due to antibiotic tolerance and biofilm formation. Lactoferrin, an iron-binding glycoprotein abundant in mammals’ secretions and neutrophil granules, has emerged as a promising multifunctional agent that could help manage staphylococcal skin and wound infections, as it combines direct antimicrobial activity with immunomodulatory and tissue-repair effects. This mini-review aims to synthesize current evidence on the role of lactoferrin in the prevention and treatment of staphylococcal skin and wound infections, focusing on its antimicrobial mechanisms, modulation of host responses, and therapeutic applications. In vitro studies demonstrate that lactoferrin inhibits S. aureus growth through iron sequestration and membrane disruption, and it can also disrupt biofilm formation and persistence. Additionally, experiments showed that lactoferrin modulates inflammation, reduces oxidative stress, and promotes fibroblast migration and collagen deposition, facilitating wound closure. Lactoferrin incorporated into hydrogels, films, or nanocarriers enhanced antibacterial activity and synergized with antibiotics or bacteriophages in preclinical models. Nonetheless, variability in dosing, formulation, and study design limits cross-study comparisons, and potential bacterial resistance mechanisms remain underexplored. Therefore, further controlled and standardized studies are needed in order to optimize clinical translation and integration into modern wound care.