title: Phototherapeutic hardening modulates systemic cytokine levels in patients with polymorphic light eruption.
abstract: The etiopathogenesis of polymorphic light eruption (PLE) has been linked to impaired UV-immunosuppression, Langerhans cell (LC) retention, and an absence of neutrophil infiltration into UV-exposed PLE skin. We have previously shown that photohardening restores the impaired neutrophil responsiveness to the chemoattractants leucotriene B4 and formyl-methionyl-leucyl-phenylalanin in PLE patients. The aim of this study was to investigate whether photohardening modulates baseline chemokine and cytokine levels which would alter chemoresponsiveness and hence immune function in PLE patients. Sixteen PLE patients received photohardening therapy for 4-9 weeks by 311 nm UVB. Plasma samples were taken both before and within 48 h of the penultimate phototherapeutic exposure. Plasma from these 16 patients, 8 non-irradiated PLE patients, and 14 control subjects was analyzed for IL-1β, CXCL8 (IL-8), IL-10, IL-17, TNF, CCL2 (MCP-1), CCL5 (RANTES), CCL11 (eotaxin), and CCL22 (MDC). These cytokines and chemokines were measured in early spring (March to April) and again in late spring (April to June). PLE patients had a significantly elevated level of CCL11 (p = 0.003) and IL-1β (p = 0.002) in early spring (before phototherapy). In late spring, after phototherapy, PLE patients had significantly elevated CCL2 (p = 0.002) and TNF (p = 0.002) but a trend for lowered plasma levels of CXCL8 (p = 0.021). When comparing the cytokine shifts from early to late spring, while healthy controls and non-UV-irradiated PLE patients showed an increase, PLE patients undergoing photohardening exhibited a trend for decrease in IL-1β (p = 0.012). Taken together, our results indicate that photohardening may alter the complex cytokine milieu in PLE, in particular via IL-1β, helping to normalise the pathophysiologic response to subsequent UV exposure.
authors.affiliation: Research Unit for Photodermatology, Department of Dermatology, Medical University of Graz, Auenbrugger Platz 8, A-8036 Graz, Austria. peter.wolf@medunigraz.at
authors.forename: Peter
authors.initials: P
authors.lastname: Wolf
authors.forename: Alexandra
authors.initials: A
authors.lastname: Gruber-Wackernagel
authors.forename: Beate
authors.initials: B
authors.lastname: Rinner
authors.forename: Antonia
authors.initials: A
authors.lastname: Griesbacher
authors.forename: Katharina
authors.initials: K
authors.lastname: Eberhard
authors.forename: Andrea
authors.initials: A
authors.lastname: Groselj-Strele
authors.forename: Gerlinde
authors.initials: G
authors.lastname: Mayer
authors.forename: Rudolf E
authors.initials: RE
authors.lastname: Stauber
authors.forename: Scott N
authors.initials: SN
authors.lastname: Byrne
mesh_terms: D000293:Adolescent; D000328:Adult; D054413:Chemokine CCL11 / Q000097:blood; D018932:Chemokine CCL2 / Q000097:blood; D018925:Chemokines / Q000097:blood*; D016207:Cytokines / Q000097:blood*; D005260:Female; D006801:Humans; D053583:Interleukin-1beta / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008297:Male; D008875:Middle Aged; D010787:Photosensitivity Disorders / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D010789:Phototherapy; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D014466:Ultraviolet Rays; D055815:Young Adult
chemical_list: D054413:Chemokine CCL11; D018932:Chemokine CCL2; D018925:Chemokines; D016207:Cytokines; D053583:Interleukin-1beta; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha