Altered expression of interleukin 6 and interleukin 10 as a result of photodynamic therapy in vivo

• Published in: Cancer research (Chicago, Ill.) Vol. 57; no. 18; pp. 3904 - 3909
• Main Authors: GOLLNICK, S. O, LIU, X, OWCZARCZAK, B, MUSSER, D. A, HENDERSON, B. W
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Association for Cancer Research 15.09.1997
• Subjects: Animals; Biological and medical sciences; Cytokines - genetics; Gene Expression Regulation, Neoplastic - drug effects; Hematoporphyrin Derivative - pharmacology; Interleukin-10 - genetics; Interleukin-10 - metabolism; Interleukin-6 - genetics; Interleukin-6 - metabolism; Mammary Neoplasms, Experimental - drug therapy; Medical sciences; Mice; Mice, Inbred BALB C; Photochemotherapy; Photoradiation therapy and photosensitizing agent; RNA, Messenger - genetics; RNA, Neoplasm - genetics; Spleen - metabolism; Time Factors; Treatment with physical agents; Treatment. General aspects; Tumor Cells, Cultured; Tumors; Ultraviolet Rays; Immune response; Immunomodulation; Rodentia; Cytokine; Cellular immunity; Malignant tumor; Mechanism; Phototherapy; Interleukin 6; Vertebrata; Experimental disease; Mammalia; Treatment; Mouse; Animal; Interleukin 10
• ISSN: 0008-5472; 1538-7445

Photodynamic therapy (PDT), which can effectively destroy malignant tissue, also induces a complex immune response that potentiates antitumor immunity but also inhibits skin contact hypersensitivity (CHS) and prolongs skin graft survival. The underlying mechanisms responsible for these effects are poorly understood but are likely to involve mediation by cytokines. We demonstrate in a BALB/c mouse model that PDT delivered to normal and tumor tissue in vivo causes marked changes in the expression of cytokines interleukin (IL)-6 and IL-10 but not tumor necrosis factor alpha. IL-6 mRNA and protein are strongly enhanced in the PDT-treated EMT6 tumor. PDT also increased IL-6 mRNA in exposed spleen and skin. These data suggest that the general inflammatory response to PDT may be mediated at least in part by IL-6. In addition, IL-6 may modulate the local antitumor immune response. In contrast, IL-10 mRNA in the tumor decreases following PDT. Most importantly, IL-10 is markedly induced in the skin of mice exposed to a PDT regime that strongly inhibits the CHS response, and the kinetics of IL-10 induction coincide with the known kinetics of CHS inhibition. We propose that the enhanced IL-10 expression plays a role in the observed suppression of cell-mediated responses seen following PDT.