Topical photodynamic therapy induces systemic immunosuppression via generation of platelet-activating factor receptor ligands
Abstract
Photodynamic therapy (PDT) is an FDA-approved procedure used for the treatment of pre-cancerous actinic keratosis as well as superficial skin cancers (Morton et al, 2008). The treatment is based on the topical application of a photosensitizing agent or its metabolic precursor (e.g. 5-aminolevulinic acid; 5-ALA) that has preferential uptake by proliferative/metabolically active cells (e.g. malignant cells), followed by exposure of the treated skin to a light source of a specific wavelength. This exposure promotes the photosensitizing agent to generate singlet oxygen and then other reactive oxygen species, leading to oxidative stress and cell death (Dougherty et al, 1998). Several studies have shown that PDT can cause immunosuppression in both humans and mice, but the mechanisms underlying these effects are not totally clear (Matthews and Damian, 2010, Mroz and Hamblin, 2011).
Platelet-activating factor (1-alkyl-2-acetyl glycerophosphocholine; PAF) is a lipid-derived mediator with diverse functions. Glycerophosphocholines (GPCs) from cell membranes can undergo oxidation resulting in the formation of oxidized GPCs (Ox-GPCs) which can act as potent agonists for the PAF receptor (PAF-R) (Konger et al, 2008). Numerous environmental pro-oxidative stressors from cigarette smoke to ultraviolet B radiation (UVB) can induce systemic immunosuppression via generation of Ox-GPC PAF-R ligands (Sahu et al, 2013, Walterscheid et al, 2002, Wolf et al, 2006, Yao et al, 2009, Zhang et al,…
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