Histochemical evidence for induction of arachidonate 15-lipoxygenase in airway disease

We have previously described the distribution of the arachidonate 15- lipoxygenase in lung tissue obtained from healthy human subjects. In the present study, we have utilized the same immunohistochemical methodology to examine the expression of 15-lipoxygenase in bronchial biopsy tissue from subjects with airway disease. Immunohistochemistry of bronchial tissue using two antibodies against distinct epitopes of the 15-lipoxygenase and indirect biotin-avidin-peroxidase detection demonstrated that, in contrast to airway tissue from normal subjects (n = 10) in which 15-lipoxygenase antigen was confined to the uppermost airways (nose and trachea) and was almost undetectable in bronchi, the bronchial tissue obtained from subjects with asthma (n = 7) or chronic bronchitis (n = 7) exhibited markedly positive immunostaining of mucosal epithelial cells with both anti-15-lipoxygenase antibodies. Specificity of 15-lipoxygenase immunostaining was verified by antigen competition experiments and by the lack of immunostaining with preimmune serum or control anti-5-lipoxygenase antibodies. The increased levels of 15-lipoxygenase antigen in the bronchial epithelial cells of asthmatic and bronchitic subjects compared with the same cell population in normal subjects coupled with the previous findings of increased 15- lipoxygenase activity in asthmatic airways suggest that epithelial 15- lipoxygenase is induced by airway inflammatory disease.