The effect of
Z-100, a
lipid-
arabinomannan extracted from Mycobacterium tuberculosis strain Aoyama B, was investigated on the resistance of thermally injured mice (TI-mice) to herpes simplex virus type 1 (HSV)
infections. The susceptibility of TI mice to
infection was about 100 times greater than it was in normal mice (N mice). However, the increased susceptibility of TI mice to
infection was effectively counteracted to the levels observed in N mice when treated with
Z-100 (10 mg/kg i.p.; 1, 3 and 5 days after thermal injury). Adoptive transfer of
burn-associated CD8+ CD11b+
TCR gamma/delta + suppressor T (BAST) cells, prepared from TI mice, increased the susceptibility of N mice to
infection by HSV, while the susceptibility of N mice, inoculated with the CD8+ T-cell fraction prepared from Z-100-treated TI mice (ZTC), to
infection was not changed. In addition, the suppressor cell activity of BAST cells was not demonstrated when they were assayed in vitro in the presence of anti-IL-4
monoclonal antibody (mAb). BAST cells released
IL-4 into their culture fluids without stimulation. The suppressor cell activity of ZTC and
IL-4 production by ZTC were minimal. These results suggest that
Z-100 may improve the resistance of TI mice to HSV
infection through the regulation of BAST cells and/or the release of
IL-4 from these cells.