Abstract
Macrophages (MØs) are known to produce various arachidonic acid (AA) metabolic products, which may either enhance or suppress inflammatory processes. 1, 2 The amount and type of AA metabolites differ according to the state of activation of the MØ. 1-3 In animal models, immunologically activated MØs produce fewer cyclooxygenase (CO) and lipoxygenase (LO) products than resident MØs. 3-4 Limited data exist, however, concerning AA metabolism by human alveolar MØs (AMs). Since activated AMs appear to be important in the pathogenesis of pulmonary sarcoidosis and idiopathic pulmonary fibrosis (IPF), we investigated AA metabolism by AMs obtained from patients with these interstitial lung diseases.
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