Effect of in vitro inoculation of bovine respiratory syncytial virus on bovine pulmonary alveolar macrophage function.

Viruses may predispose the respiratory tract to the development of secondary bacterial pneumonia by impairing functions of alveolar macrophages. The effects of bovine respiratory syncytial virus (BRSV) on selected functions of bovine pulmonary alveolar macrophages (PAM) were examined in vitro. Alveolar macrophages were obtained from nonsedated cattle, using a polypropylene tube passed intranasally into the lung. The PAM lavaged from the lung were allowed to adhere to glass coverslips or plastic tissue culture plates, and were exposed to BRSV for 2 hours. Control and BRSV-inoculated PAM were compared at intervals over a 72-hour period for their abilities to phagocytize and kill Staphylococcus epidermidis, rosette with and phagocytize antibody-coated sheep RBC (SRBC), phagocytize latex particles, and influence lysosomal enzyme activity. Challenge exposure with BRSV did not affect the ability of PAM to adhere and did not affect cell viability. There were numerical differences between control and BRSV-inoculated cell populations in phagocytosis and killing of S epidermidis, but these were not significant (P greater than 0.05). There was less than 5% difference in the abilities of control and BRSV-challenged PAM to phagocytize latex beads. When Fc-receptor-mediated phagocytosis of antibody-coated SRBC was compared with controls, BRSV-challenged PAM had significantly (P less than 0.05) impaired phagocytic function, which was maximal 72 hours after BRSV inoculation; the phagocytic impairment occurred in spite of normal Fc-receptor function, as determined by rosetting with antibody-coated SRBC.(ABSTRACT TRUNCATED AT 250 WORDS)

Regulation of canine platelet function II. Catecholamines.

The action of epinephrine (E) on canine platelet aggregation is described. Although E did not induce a change in platelet shape or aggregation, potentiation of aggregation induced by the following agents was observed at physiological E concentrations (that is, less than 10 nM/1): arachidonic acid; the dense granule agonists, ADP and serotonin (5-HT); and collagen. Epinephrine-induced potentiation was in part independent of formation of arachidonic acid metabolites, and E potentiated the aggregating action of the bivalent cationophore A23187. Potentiation was inhibited by alpha-adrenergic receptor antagonists phenoxybenzamine, phentolamine, and ergotamine, and mimicked by alpha-adrenergic receptor agonists norepinephrine, clonidine, and in some cases, phenylephrine. The beta-adrenergic receptor agonists isoproterenol and dobutamine inhibited ADP-induced aggregation, and this action was presented by pretreating the platelets with propranolol and dichloroisoproterenol. An augmentation of the aggregation response of platelets to arachidonic acid was observed in blood samples withdrawn when circulating catecholamines were elevated. The physiological implication of epinephrine acting as a gain controller that alters the relationship between actuating signal and the platelet response to an agonist is discussed.