Role for T lymphocytes in silica-induced pulmonary inflammation

The role of the immune system in modulating pulmonary damage evoked by exposure to silica crystals has been examined in a mouse model of experimental silicosis. Congenitally T cell-deficient mice (Balb/c nu/nu) were compared with T cell sufficient mice (Balb/c nu/+) in the degree of silica-induced cellular inflammation on days 3, 5, 7, 30, and 60 after an intratracheal instillation of silica. Cellular inflammation was assessed by increases in the total number and type of inflammatory cell in lung lavage fluid and in lung tissue. Inflammation and/or injury were also measured in the lavage fluid by increases in total protein, angiotensin-converting enzyme and plasminogen activator. No significant difference existed between the two types of mice in total lavage cell number or total protein. In nu/+ mice, the neutrophil predominated early, followed by the macrophage as the major inflammatory cell. However, in nu/nu mice, the neutrophil remained the predominant inflammatory cell throughout the two months postinjection. In addition, angiotensin-converting enzyme levels remained elevated in the nu/nu animals above those in the nu/+ mice whereas plasminogen activator was elevated early (before day 7) in both, and decreased comparably over time. These data suggest that T cells directly or indirectly influence the maintenance of a macrophage infiltrate and the termination of a neutrophil response after exposure to silica. However, it appears that neither T cells nor the cells they influence affect the ultimate amount of collagen deposition.