Effects of skin ultraviolet light exposure on Staphylococcus aureus cutaneous infection

ELIANA M. CELA; CINTIA GONZALEZ; ADRIAN D. FRIEDRICH; CAMILA LEDO; JULIANA LEONI; MARISA GOMEZ; DANIEL H. GONZALEZ MAGLIO

Mar del Plata

Congreso; LXII Reunión Anual Sociedad Argentina de Inmunología; 2014

Sociedad Argentina de Inmunología

It is well known that ultraviolet radiation (UVr) leads to immunosuppression, inhibiting contact hypersensitivity (CHS) reactions. However, the way UVr modulates immune responses againstmicroorganisms has been poorly explored. Considering that Staphylococcus aureus (SA) causes skin infections and this organ is the main target of UVr, our aim was to evaluate if UVr canmodulate the host response to SA infection. We compared 2 types of exposures: a single high UV dose (shUVd - 400 mJ/cm2), simulating a harmful exposure vs. repetitive low UV doses (rlUVD- 4 consecutive days, 20 mJ/cm2), simulating daily exposures. Previously, we have found that shUVd promotes skin inflammation while it diminishes CHS reaction, in contrast to rlUVd that does not induce inflammation and increases CHS response. SKH:1 hairless mice (n=6) were irradiated and 24h later were inoculated with SA strain LAC (1x107 CFU). Non-irradiated mice were used as control (C). The infection was monitored by measuring the abscess size and mice weight daily. Six days p.i., mice were bled and sacrificed. Skin abscess and spleen were removed and homogenized to perform bacterial counts. Specific cell responses were determined in vitro stimulating spleen cells with 1x107 CFU/well of heat killed bacteria. Finally, the titer of specific IgG was determined in sera samples. No differences in weight, abscess size and bacterial counts were found. shUVd mice did not show differences in the dissemination of bacteria or in spleen cells proliferative response, whereas they produced higher titers of specific IgG (p<0,05 vs C). Contrariwise, rlUVd mice showed a marked increase in the dissemination of bacteria (p<0,05 vs C) and specific proliferative responses (p<0,05 vs C), but did not present differences in specific IgG titers. These results show that UVr may modulate SA skin infection, depending on the type ofexposure. To our knowledge, this is the first report evaluating the relationship among UVr, infection and immunity.