Levamisole-induced attenuation of alveolar macrophage dysfunction in respiratory virus-infected calves.

A luminol-amplified chemiluminescence (CL) assay was used to evaluate the effect of levamisole on the metabolic activity of pulmonary alveolar macrophages (PAM) from parainfluenza-3 (PI-3) and infectious bovine rhinotracheitis (IBR) virus-infected calves. Using selective beta-adrenergic agonists and antagonists, beta 1-adrenoceptors were shown to inhibit the PAM reactive oxygen species-dependent CL response. Beta 2 adrenoceptors were apparently not important in the regulation of CL in PAM of control calves. Infection of calves with IBR virus significantly impaired beta 1-receptor function. PI-3 virus infection, in addition to disrupting beta 1-receptors, also unmasked PAM beta 2-receptor activity. Treatment of calves with levamisole, 3 mg/kg, sub-cutaneously, partially reversed the virus-induced impairment of PAM beta 1-receptor function without influencing beta 2-receptor activity. In conclusion, beta-adrenoceptors regulate bovine PAM CL response. Pulmonary viruses impair PAM beta 1-receptor function, an action which can disrupt pulmonary homeostasis. Levamisole partially restores beta-receptor effects on PAM, and may therefore be useful in the management of virus-associated bacterial pneumonia.