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Keywords:

  • UVR;
  • ultraviolet radiation;
  • MLM;
  • Mycobacterium lepraemurium;
  • DTH;
  • delayed-type hypersensitivity;
  • AFB;
  • acid-fast bacteria

Abstract The purpose of this study was to determine whether exposing mice to ultraviolet radiation (UVR) would alter the pathogenesis of infection with Mycobacterium lepraemurium (MLM), which causes a chronic, progressive, lethal disease in susceptible mouse strains. BALB/c mice were irradiated on dorsal skin with various doses of UVR from FS40 sunlamps 3 days before infection with MLM in the hind footpad. The course of disease was followed by assessing the number of acid-fast bacteria in the footpad, regional lymph node and spleen, and measuring the size of the lesion at the site of MLM infection at various times after infection. Mice were also tested periodically for a delayed-type hypersensitivity (DTH) response by injecting MLM antigen into the uninfecled footpad and measuring footpad swelling 24 hours later. Mice treated with a single high dose of UVR (45 kJ/m2) had significantly more bacteria in the infected footpad, lymph node and spleen than unirradiated control animals. They also had larger lesions at the site of MLM infection and exhibited significant suppression of the DTH response at 3 and 6 months after infection. Injection of mice s.c. in the footpad with MLM 3 d after 45 kJ/m2 UVR reduced the median survival time from 391 to 305 d and after i.v. infection from 171 to 139 d. Dose-response studies indicated that exposing mice to 2.3 kJ/m2 of UVR, which is approximately 1 minimal erythemal dose for this strain, suppressed the DTH response by 50% at 3 months alter infection. Significant increases in the number of bacteria in the footpad, spleen and lymph node were detected with doses of UVR≥5.6 kJ/m2. Mice exposed chronically to UV radiation also showed impaired responses to MLM. Thus, exposing mice to a single or multiple doses of UVR before infection increased the severity of a chronic mycobacterial infection and decreased the immune response to mycobacterial antigens.