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Published on: March 25, 2020
Oestrogen promotes healing in a bacterial LPS model of delayed cutaneous wound repair
Rachel Crompton1, Helen Williams1, David Ansell1,2
1The Healing Foundation Centre, Faculty of Life Sciences, The University of Manchester, Manchester, UK.
Abstract:
Wound infection is a major clinical problem, yet understanding of bacterial host interactions in the skin remains limited. Microbe-derived molecules, known as pathogen-associated molecular patterns, are recognised in barrier tissues by pattern-recognition receptors. In particular, the pathogen-associated molecular pattern, lipopolysaccharide (LPS), a component of microbial cell walls and a specific ligand for Toll-like receptor 4, has been widely used to mimic systemic and local infection across a range of tissues. Here we administered LPS derived from Klebsiella pneumoniae, a species of bacteria that is emerging as a wound-associated pathogen, to full-thickness cutaneous wounds in C57/BL6 mice. Early in healing, LPS-treated wounds displayed increased local apoptosis and reduced proliferation. Subsequent healing progression was delayed with reduced re-epithelialisation, increased proliferation, a heightened inflammatory response and perturbed wound matrix deposition. Our group and others have previously demonstrated the beneficial effects of 17β-estradiol treatment across a range of preclinical wound models. Here we asked whether oestrogen would effectively promote healing in our LPS bacterial infection model. Intriguingly, co-treatment with 17β-estradiol was able to promote re-epithelialisation, dampen inflammation and induce collagen deposition in our LPS-delayed healing model. Collectively, these studies validate K. pneumoniae-derived LPS treatment as a simple yet effective model of bacterial wound infection, while providing the first indication that oestrogen could promote cutaneous healing in the presence of infection, further strengthening the case for its therapeutic use.
Insights
This study shows that lipopolysaccharide (LPS) from Klebsiella pneumoniae delays wound healing. However, 17β-estradiol treatment can reverse these effects, promoting healing even with bacterial infection.
Area of Science:
- Dermatology
- Immunology
- Microbiology
Background:
- Wound infection is a significant clinical challenge with limited understanding of bacterial-host interactions in skin.
- Pathogen-associated molecular patterns (PAMPs), like lipopolysaccharide (LPS), are recognized by pattern-recognition receptors, influencing tissue responses.
- Lipopolysaccharide (LPS) from Klebsiella pneumoniae is an emerging wound pathogen.
Purpose of the Study:
- To establish a mouse model of cutaneous wound infection using Klebsiella pneumoniae-derived LPS.
- To investigate the effects of LPS on wound healing processes, including cellular proliferation, apoptosis, inflammation, and matrix deposition.
- To evaluate the therapeutic potential of 17β-estradiol in promoting wound healing during LPS-induced bacterial infection.
Main Methods:
- Administration of Klebsiella pneumoniae-derived LPS to full-thickness cutaneous wounds in C57/BL6 mice.
- Assessment of wound healing parameters, including re-epithelialisation, proliferation, apoptosis, inflammation, and collagen deposition.
- Evaluation of co-treatment with 17β-estradiol on LPS-impaired wound healing.
Main Results:
- LPS treatment led to increased apoptosis and reduced proliferation in early wound healing.
- Delayed healing progression was observed, characterized by reduced re-epithelialisation, increased proliferation, heightened inflammation, and altered matrix deposition.
- Co-treatment with 17β-estradiol significantly improved re-epithelialisation, reduced inflammation, and increased collagen deposition in LPS-treated wounds.
Conclusions:
- Klebsiella pneumoniae-derived LPS provides a viable model for studying bacterial wound infection.
- 17β-estradiol demonstrates therapeutic potential in promoting cutaneous wound healing in the presence of bacterial infection.
- Estrogen's role in enhancing wound healing during infection warrants further investigation for clinical applications.
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