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Microbial elements as the initial triggers in the pathogenesis of polymorphic light eruption?
VijayKumar Patra1,2, Peter Wolf2
1Center for Medical Research, Medical University of Graz, Graz, Austria.
Abstract:
The primary trigger of polymorphic light eruption (PLE) remains to be uncovered. We hypothesize that PLE may be initiated by elements resulting from UV-induced damage to microbial communities of the skin, leading to a cascade of events eventually resulting in the skin rash of the disease. One mechanism by which epidermal injury by UV radiation could trigger PLE are danger signals such as damage or pathogen associated molecular patterns DAMP/PAMPs or commensal-associated molecular patterns (CAMPs). Such triggers could be produced due to UV-induced stress on microbial communities of the skin and exacerbate inflammatory responses by inducing the innate immune system through antimicrobial peptides (AMPs) such as psoriasin, RNase7, HBD-2 and LL-37. These AMPs also actively take part in initiating adaptive immunity. That signals derived from microbial rather than human elements may initiate PLE is supported by series of observations, including the PLE-protective effect of topically applied microbial-derived DNA repair enzymes.
Insights
Polymorphic light eruption (PLE) may be triggered by UV-induced damage to skin microbes. This damage releases microbial signals that activate the innate immune system, causing the characteristic rash.
Area of Science:
- Dermatology
- Immunology
- Microbiology
Background:
- The precise trigger for polymorphic light eruption (PLE) is unknown.
- This study hypothesizes that UV radiation damages skin's microbial communities, initiating PLE.
- UV-induced damage may release microbial danger signals (DAMPs/PAMPs/CAMPs) that activate the innate immune system.
Discussion:
- UV radiation can stress skin microbes, leading to the release of damage- or pathogen-associated molecular patterns (DAMPs/PAMPs) and commensal-associated molecular patterns (CAMPs).
- These microbial signals can activate the innate immune system via antimicrobial peptides (AMPs), such as psoriasin, RNase7, HBD-2, and LL-37.
- AMPs play a role in both innate and adaptive immunity, potentially contributing to PLE pathogenesis.
Key Insights:
- Evidence suggests microbial, not human, elements may trigger PLE.
- Topical application of microbial DNA repair enzymes has shown a protective effect in PLE.
- This supports the hypothesis that UV-induced microbial damage is a key factor in PLE.
Outlook:
- Further research is needed to elucidate the specific microbial triggers and immune pathways involved in PLE.
- Investigating the role of the skin microbiome in PLE pathogenesis could lead to novel therapeutic strategies.
- Targeting UV-induced microbial damage or modulating the skin microbiome may offer new avenues for PLE prevention and treatment.
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