Immunoglobulin responses to experimental silicosis

Silicosis is a crippling fibrotic lung disease induced by inhalation of cry stalline silica. One feature of silicosis is systemic and pulmonary immune dysfunction characterized in part by elevations in serum and bronchoalveola r lavage (BAL) immunoglobulins. A major specific aim of the current report was to demonstrate that an experimental model of silicosis previously well characterized for the development of pulmonary inflammation and fibrosis wo uld also exhibit increased levels of serum and BAL. IgG and IgM similar to those of human silicosis. We also sought to document the anatomic compartme nts responsible for these immunoglobulin responses. To address these specif ic aims, we compared levels of IgG and IgM in serum and BAL from rats with experimental silicosis induced by inhalation of silica with levels of these immunoglobulins in titanium dioxide (TiO2)- and sham (air)-exposed control s. The ability of mononuclear cell populations from lung, lung-associated l ymph node, and spleen to produce IgG and IgM ex Five were also compared. We found that experimental silicosis was associated with elevated IgG and IgM levels in blood and BAL relative to the control groups. Our findings also suggested that draining lung-associated lymph nodes (LALN) were the most im portant sites for increased IgG and IgM production in experimental silicosi s, with lungs contributing to a lesser degree. Increased production in the LALN appeared related to marked expansion in total numbers, but not relativ e proportion, of B lymphocytes.