Tenascin expression and distribution in pleural inflammatory and fibrotic diseases

We hypothesized that tenascin expression is increased in pleural inflammato ry and fibrotic diseases and that its expression can be used as a marker of active pleural involvement. For this purpose we analyzed 71 histological s amples of inflammatory and fibrotic pleura from patients with asbestos-indu ced pleural reaction (n = 6), postcardiac injury syndrome (n = 6), parapneu monic infection and/or empyema (n = 23), tuberculosis (n = 5), rheumatoid d isease (n = 1), and fibrosis with inflammation of unknown etiology (n = 30) . All 71 cases were studied by immunohistochemistry for tenascin. In 19 sel ected cases tenascin mRNA in situ hybridization was also performed. In ever y case, tenascin was increased by immunohistochemistry. Most prominent immu noreactivity was detected in areas of newly formed fibrosis. Increased tena scin mRNA expression by in situ hybridization was detected in the individua l cells of the newly formed fibrosis underneath the fibrinous exudate. The tenascin mRNA-positive cells localized in areas in which by immunohistochem ical studies the cells were positive for alpha-smooth muscle actin, desmin, and vimentin, suggesting a myofibroblast phenotype. Tenascin mRNA expressi on was also seen less frequently in areas in which some cells were positive for cytokeratin. These cells might represent: mesothelial cells entrapped in the inflammatory lesion. Alternatively, they might represent fibroblast- type cells with aberrant cytokeratin expression. We conclude that in pleura l inflammatory and fibrotic diseases tenascin immunoreactivity is increased and tenascin mRNA-positive cells localized mainly in the areas of myofibro blast- and, less often, mesothelial-type cells, suggesting that mainly myof ibroblasts and, less commonly, also mesothelial cells might be responsible for tenascin expression in pleural inflammatory and fibrotic diseases.