Modulation of immunologic responses in nontuberculous mycobacterial infections with indomethacin.
We have previously reported that impaired in vitro cellular immunity is a common finding in patients with nontuberculous mycobacterioses and that the subnormal responses may be improved by indomethacin. Subsequently, we have studied the in vivo effects of indomethacin on cell-mediated immune functions of four patients with Mycobacterium avium-intracellulare infections. Prior to treatment none of the patients had delayed cutaneous reactions to purified protein derivative (PPD) of the tubercle bacillus, and their lymphocytes had subnormal in vitro proliferation responses to tuberculins from M. tuberculosis and M. avium-intracellulare and to phytohemagglutinin. The administration of indomethacin reconstituted both the in vitro lymphocyte responses and delayed cutaneous hypersensitivity. We propose that the impairment of T-cell dependent immune functions is mediated by a suppressive factor (or factors) that is a metabolic product(s) of the cyclooxygenase pathway of arachidonic acid metabolism. Preferential inhibition of this pathway with indomethacin allows the expression of cell-mediated responses.
D003876:Dermatitis, Atopic / Q000188:drug therapy; D006801:Humans; D006968:Hypersensitivity, Delayed / Q000188:drug therapy; D007111:Immunity, Cellular / Q000187:drug effects; D007213:Indomethacin / Q000627:therapeutic use*; D008213:Lymphocyte Activation; D009164:Mycobacterium Infections / Q000276:immunology*; D009165:Mycobacterium Infections, Nontuberculous / Q000276:immunology*; D010865:Pilot Projects; D012882:Skin Tests
D007213:Indomethacin