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

Abstract

SummaryBackgroundPolymorphic light eruption (PLE) has been attributed to type IV, most likely delayed‐type hypersensitivity response (adaptive immunity) but little is known on innate immunity, especially antimicrobial peptides (AMPs) in the disease. Abnormalities in AMP expression have been linked to pathological skin conditions such as atopic dermatitis (AD) and psoriasis.MethodsAntimicrobial peptide profiling was carried out in PLE skin samples (n,12) compared with that of healthy (n,13), atopic (n,6), and psoriatic skin (n,6).ResultsCompared to healthy skin, we observed increased expression of psoriasin and RNAse7 (both mostly in stratum granulosum of the epidermis), HBD‐2 (in the cellular infiltrate of the dermis), and LL37 (mostly in and around blood vessels and glands) in PLE lesional skin, a similar expression profile as present in psoriatic skin and different to that of AD (with little or no expression of psoriasin, RNAse7, HBD‐2, and LL37). HBD‐3 was downregulated in PLE compared to its high expression in the epidermis and dermis of healthy skin, AD, and psoriasis.ConclusionThe unique profile of differentially expressed AMPs in PLE implies a role in the pathophysiology of the disease, possibly directly or indirectly linked to the microbiome of the skin.

Desired response to phototherapy vs photoaggravation in psoriasis: what makes the difference?

“…Similar to photosensitive rosacea, in which LL‐37 increases UVB‐triggered inflammasome activation, this AMP may also play a role in PLE‐koebnerized psoriasis as we found it to be significantly increased in blood vessels in the dermis of lesional PLE skin compared to healthy skin (Fig. c) . This is consistent with the observation that LL‐37 expression is commonly increased in psoriasis and other inflammatory diseases such as lupus erythematosus and contact dermatitis, but downregulated in atopic dermatitis .…”

“…TLRs can also regulate AMP expression, and laboratory studies have shown that exposure to UV can induce the AMPs human beta‐defensin (HBD) 2, HBD3, RNAse7 and S100A7 (psoriasin) by keratinocytes in vitro and in vivo . Intriguingly, exposure to UV can lead to upregulation of AMP in an atypical manner in patients with PLE when compared to healthy subjects . Importantly, topical treatment with vitamin D3 analogues such as calcipotriol, known to suppress cellular immune response through expansion of Tregs, has been found to decrease the expression of AMPs including HBD2 and psoriasin in psoriatic skin (cited in Ref.…”

Polymorphic Light Eruption: What's New in Pathogenesis and Management

“…Patra et al have found that the expression of psoriasin, RNase7, HBD-2, and LL-37 was increased in PLE lesional skin, whereas HBD-3 was decreased. Considering the skin surface as a “multiethnic world,” without forgetting the crucial role of keratinocytes, we can't exclude that AMPs release could be determined by modification in microbiome components after UV interaction ( 23 ). Indeed, microbiome could represent the source, direct or indirect, of the yet undetected UVR-induced antigens formed in PLE patients, leading to keratinocyte damage.…”

“…Indeed, microbiome could represent the source, direct or indirect, of the yet undetected UVR-induced antigens formed in PLE patients, leading to keratinocyte damage. As a consequence, LL-37, also induced by UVB, IFNγ, TNF-α, IL-6, could represent a potential indirect driver of PLE ( 23 ). It can form aggregates with self-nucleic acids able to activate pDCs: in psoriasis it has been recognized as the main autoantigen ( 24 ).…”

Resolution of plaque-type psoriasis: what is left behind (and reinitiates the disease)

“…Might a nerve scar left behind after successful treatment contribute to the reappearance of psoriatic lesions, be it during or after continuous treatment? Last but not the least, may the interplay of the microbiome and AMPs [85,86] help trigger psoriatic recurrence? This may be in particular important for pustular psoriasis, in which IL-1/IL-36 plays an important role in the pathogenesis [87][88][89].…”