Interesting Lyme study with mice and UV exposure

Discussion in 'Lyme Disease Archives' started by jarjar, Oct 15, 2006.

  1. jarjar

    jarjar New Member

    INTRODUCTION

    Borrelia burgdorferi (Bb)', the causative agent of Lyme disease (LD), is transmitted during the blood meal of infected ticks to humans and other mammals (1). The tick bite can result in a local rash that can be followed by a flu-like illness. Successful antibiotic treatment is contingent on early diagnosis of the disease; however, untreated Lyme borreliosis can result in late manifestations that can include arthritis, meningitis, cardiac disease and neurological symptoms (2). Although both cellular and humoral responses to Borrelia have been documented, the host immune responses to this organism are incompletely understood (2).

    Our laboratory has been engaged in characterizing the effects of ultraviolet (UV) exposure on marine immune responses to various microbial pathogens and other antigens (3-7). Exposing the skin of these mice to UVR reduced both contact-hypersensitivity (CHS) responses and delayed-typehypersensitivity (DTH) responses to antigens introduced at unexposed sites (8,9). In addition, antigen-specific T-suppressor cells were generated following immunization of the UV-irradiated host (10,11). Previous work has demonstrated that cytokines and biological-response modifiers released by UV-irradiated keratinocytes, specifically interleukin (IL)-10, tumor necrosis factor (TNF)-a and cis-urocanic acid, mediated the systemic, immunosuppressive effects induced by UV irradiation (12,13). Furthermore, alterations in the activity of antigen-presenting cells in the central lymphoid organs appeared to be the mechanism underlying immune suppression (14,15). This systemic effect of UV irradiation also suppressed the DTH response to Mycobacterium bovis, Mycobacterium lepraemurium and Candida albicans in mice (5,6,16-18). In marine infectious-disease models for malaria and influenza UV-induced alterations to the levels of IL-10 and TNF-a, respectively, were associated with increased mortality following infection with these agents (19-21). Furthermore, depending on the timing of irradiation with respect to herpes-simplex infection, infected and irradiated rats presented either impaired cellular responses or large increases in the quantity and severity of the lesions (22).

    Our initial studies tested the hypothesis that systemic effects of UV irradiation shifted the balance of the immune response from Thl- to Th2-type responses (3). Thl cells are T lymphocytes that secrete primarily IL-2 and interferon (IFN)--y and serve as helper cells for DTH, CHS and the production of IgG2a and IgG2b antibody subclasses; Th2 cells secrete primarily IL-4 and IL-10 and contribute to the production of IgGI and IgE antibodies and the suppression of DTH responses (23-26). These experiments supported previous work describing roles for a UV-mediated shift from Thl- to Th2-type responses (27,28). However, recent evidence suggested that UVR could suppress both Thl- and Th2-type responses, depending on the antigens) used at the time of irradiation (29). In our model the immunizations with Borrelia in complete Freund's adjuvant induced a potent Thl response as evidenced both by a strong DTH and by IgG2a and IgG2b antibody responses to Borrelia, and these Thl responses could be diminished by UV irradiation. The Th2 antibody IgGI was increased by UV only after a secondary immunization, indicating that UV irradiation could shift, in part, the T helper lymphocyte (Th)-cell response to Borrelia (3
  2. victoria

    victoria New Member

    think this was the initial study?

    Effect of UV irradiation on infection of mice with Borrelia burgdorferi;
    Photochemistry and Photobiology, May 2001

    (Photochemistry and Photobiology is an academic publication providing coverage and analysis of science and math)

    by Brown, Eric L, Ullrich, Stephen E, Pride, Michael, Kripke, Margaret L