Microbial elements as the initial triggers in the pathogenesis of polymorphic light eruption?

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.

Unique profile of antimicrobial peptide expression in polymorphic light eruption lesions compared to healthy skin, atopic dermatitis, and psoriasis

“…In PLE, IL‐1β levels have been found to be elevated, and this could induce high psoriasin expression in the skin. Psoriasin displays a strong, selective antimicrobial activity against Escherichia coli strains, and this could theoretically hint toward the involvement of E. coli or its components in PLE lesions which is yet to be investigated …”

“…It usually occurs during spring or early summer upon exposure to sunlight and the symptoms usually subside with repeated sunlight exposure due to continuous natural photo hardening as the summer progresses or after medical photo hardening . The exact etiology and pathogenesis of PLE still remain a mystery; however, resistance to UV‐induced immunosuppression and type IV delayed‐type hypersensitivity (DTH) to photo‐antigens are believed to play a key role in the disease . The physiological occurrence of UV‐induced immunosuppression may protect healthy subjects from symptoms of PLE by suppressing the immune reaction to newly formed (photo) antigens probably due to regulatory T cells, whereas in PLE prone subjects, a failure of immune suppression might favor the occurrence of the skin rash of the disease.…”

“…Dysregulation in AMP production has been linked to many pathological skin conditions such as psoriasis, atopic dermatitis (AD), rosacea, and others . We hypothesize that there might be an overall altered expression of AMPs as well in PLE lesions induced directly by UVR or due to possible UV‐induced damage to certain microbes or microbial elements within or on the surface of the skin and such events could contribute to the pathogenesis of the disease . We herein investigate the expression of psoriasin, RNase7, HBD‐2, HBD‐3, and LL‐37, as these are the most commonly studied AMPs linked to many disease pathologies, using immunohistochemical stainings of lesional skin of PLE and compare it with that of healthy skin, lesional skin of AD and psoriasis patients.…”

Cutaneous infiltration of plasmacytoid dendritic cells and T regulatory cells in skin lesions of polymorphic light eruption

“…Recent works have also suggested that innate antimicrobial peptides (AMP) may be involved in pathogenesis of PLE . Normally, UVR‐induced AMP contributes to immunosuppression inducing Tregs, otherwise in early stages of PLE a dysregulated AMP expression following UVR could play some part in the failure of photoimmunosuppression .…”

Focus theme issue December 2016: Photobiology & photodermatology

“…Finally, Patra and Wolf contribute a Hypothesis Letter on the possible involvement of the skin's microbiome in polymorphic light eruption, while Wolf et al . examine in a viewpoint on psoriasis management by phototherapy why the latter is not always beneficial and can aggravate the condition in photosensitive patients.…”