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A rat pulmonary alveolar macrophage (PAM) cell line (NR8383) was initiated in culture in the presence of a gerbil lung cell conditioned medium (GLCM), and has been propagated continuously for over 36 mo. When examined at different times throughout this in vitro period, NR8383 exhibited characteristics typical of macrophages: (a) Zymosan ingestion was seen in 90 to 98% of the cells examined; (b) Pseudomonas aeruginosa phagocytosis in 50 to 80%; (c) Nonspecific esterase activity in greater than 95%. During the first 6 mo., the PAM replicated with doubling times approximating 15 to 20 d. Throughout this period, GLCM dependence was evident. After 27 wk in vitro, NR8383 replication increased markedly, and within 2 wk, the doubling time was less than 48 h. NR8383 was readily monitored by [3H]thymidine (TdR) blastogenesis assay. In the presence of GLCM uptake of [3H]TdR was fivefold greater than in control cultures. Adherence and growth kinetics were effectively controlled by modulation of GLCM or serum content in culture medium. It was demonstrated that PAM growth factor(s) is ubiquitous, not species-specific, and under certain conditions may be derived from "endogenous" sources of persisting non-PAM populations within the parent, uncloned line NR8383. Cloned progeny remain devoid of non-PAM "feeder" cells, but retain macrophage properties, including interleukin-1 secretion, Fc receptors, and H2O2 production.

ExtractThe saliva of patients with cystic fibrosis of the pancreas (CFP) contains higher concentrations of sodium than the saliva of normal subjects. The hypothesis that the salivary electrolyte abnormality in CFP may be due to a sodium transport inhibitory factor (or factors) present in the saliva of the~e:~atients was investigated. Such a factor would decrease sodium reabsorption in the salivary glands and cause increased sodium concentrations in the final saliva. Retrograde perfusion of the rat parotid gland was used to determine this factor. Retrograde perfusion with normal saline or saliva from normal children did not affect the rate of sodium reabsorption in the rat parotid gland. Retrograde perfusion with ouabain containing saline or saliva from patients with CFP resulted in a marked decrease of the rate of sodium reabsorption. I t was concluded that saliva from patients with CFP contains a factor that causes inhibition of sodium transport in the rat parotid gland. The similarity of the effects of ouabain and saliva from patients with CFP led us to the investigation of the possibility of a common mode of action. I t was demonstrated that the saliva of patients had no effect on the in vitro activity of membrane ATPase preparations obtained from beef parotid, human erythrocytes and rat kidneys. This indicates that the saliva of patients with CFP causes inhibition of sodium reabsorption in the rat parotid by an action other than inhibition of the activity of ATPase, an enzyme known to be involved in sodium transport across biological membranes. Speculation