We propose studies of the adverse effects of drugs commonly used in the treatment of respiratory disease which may block amplification of immune cellular defense. In tissue culture, sensitive lymphocytes and macrophages can be made to interact so as to amplify the production of MIF (macrophage inhibition factor) and LOMWIT (low molecular weight "immune transmitter") to titers of 10 to the 10th power respectively. Theophylline, isoproterenol and hydrocortisone have been reported to block MIF production or action and will therefore be added to our culture system in therapeutic concentrations to see if they block LOMWIT and MIF production or action in vitro. The mucolytic agent N-acetyl cycteine also blocks the effects of MIF. Other cycteine compounds and chemotactic agents block methylation of macrophage membrane phospholipid. Hence, the effect of MIF and N-acetyl cysteine on methylation of macrophage membrane phsopholipid by 3H-S-adenosyl methionine will be measured using already established methods. If phospholipid methylation is affected this might indicate that MIF acts by changing the stereo-chemical fluidity of the cell membrane phospholipid. It would also provide a simple, functionally relevant radio-assay for MIF. Finally, any immunosuppressive effect of N-acetyl cysteine might result from antagonism of the effect of MIF on phospholipid methylation. Massive doses (500,000) of pseudomonads are required (intratracheally) to infect healthy guinea pig lungs. Hydrocortisone (5mg/kg/day for 2-3 weeks) reduces the infective dose to 50 organisms. Similar drug/infective dose responses will be sought for theophylline, isoproterenol and N-acetyl cysteine and correlated with any effect on immune amplification in vitro. Finally LOMWIT (10 ml, titer 10 to the 4th power will be injected intraperitoneally to try and reverse drug induced susceptibility to experimental lung infection.