Antigen challenge of passively sensitized chopped human lung resulted in the generation of several arachidonic acid cyclooxygenase metabolites (AACM): thromboxane A 2 (TxA 2) as measured by its stable metabolite TxB 2, prostaglandin D 2 (PgD 2), prostacyclin (PgI 2) as measured by its table metabolite 6-keto-PgF(1α), prostaglandin F(2α) (PgF(2α)) and prostaglandin E (PgE). The kinetics of AACM release after antigen challenge paralleled histamine release. All AACM were released in an antigen dose-dependent manner and reached maximal release at antigen concentrations lower than those required for maximal histamine release. Quantitatively, of the AACM measured, PgD 2 and PgI 2 were found to predominate in anaphylactic reactions of human lung parenchyma. Generation of PgD 2 and PgI 2 were 3- to 7-fold greater than that of other AACM measured. Thromboxane B 2 was generated in quantities comparable to PgE and PgF(2α). Studies were designed to test the hypothesis that lung smooth muscle contraction per se can account for the generated AACM that are released during anaphylaxis of the lung. The studies compared antigen-induced AACM generation with methacholine-induced (10 -4M) AACM generation. The failure to confirm this hypothesis was especially evident for PgD 2 where release was dependent on mast cell activation. Thromboxane A 2, PgD 2, and PgI 2, have been reported to have potent effects on smooth muscle. Our data suggested that these AACM are generated in such sufficient quantities that they may function in important aspects of the modulation of hypersensitivity responses in human lungs.
|Original language||English (US)|
|Number of pages||5|
|Journal||American Review of Respiratory Disease|
|State||Published - Dec 6 1981|
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine