Effect of bovine herpesvirus-1 or parainfluenza-3 virus on immune receptor-mediated functions of bovine alveolar macrophages in the presence or absence of virus-specific serum or pulmonary lavage fluids collected after virus infection

The immune receptor-mediated functions of bovine alveolar macrophages (AM) inoculated in vitro with bovine herpesvirus-1 (BHV-1) or parainfluenza-3 (PI-3) virus were tested in the presence or absence of virus-specific antiserum or pulmonary lavage fluids collected from calves 6 days after inoculation with BHV-1 or PI-3 virus. The Fc and C3b phagocytic indices of noninoculated AM, collected from 6- to 16-week-old calves, ranged from 75 to 87 and 59 to 64, respectively, and the binding indices ranged from 5 to 8 and 22 to 28, respectively. Infection of AM with either BHV-1 or PI-3 virus had no significant effect on receptor-mediated phagocytosis or binding, with the exception of a significant (P < 0.05) decrease, from 64 to 46, of the C3b phagocytic index of PI-3 virus-infected AM. The addition of lavage fluids, collected after BHV-1 or PI-3 virus infection, to AM infected with the respective virus caused a significant (P < 0.05) decrease in phagocytic indices with values for the Fc and C3b indices in BHV-1-infected AM decreasing from 81 to 49 and from 47 to 8, respectively, and those for the PI-3 virus-infected AM from 79 to 51 and from 46 to 15, respectively. The binding indices of virus-infected AM increased with the addition of viral lavage fluids, but the only significant (P < 0.05) increase was for C3b binding in PI-3 virus-infected cells, which increased from 33 to 56. Virus-specific serum added to AM infected with the respective virus also caused significant (P < 0.05) decreases in the Fc and C3b phagocytic indices, with those for BHV-1-infected AM decreasing from 81 to 24 and from 47 to 5, respectively, and those for PI-3 virus-infected AM from 79 to 23 and from 46 to 3, respectively. The Fc binding index significantly (P < 0.05) increased with the addition of virus-specific serum from 8 to 34 and from 10 to 42 in BHV-1 and PI-3 virus-infected AM, respectively. The C3b binding index of these AM also increased, but not significantly. Infection of AM with either BHV-1 or PI-3 virus had no significant effect on the phagocytosis of opsonized (OPZ) or nonopsonized (nonOPZ) Staphylococcus epidermidis (SE). The addition of lavage fluids, obtained after BHV-1 infection, to AM infected with BHV-1, significantly (P < 0.05) decreased the percentage of phagocytosis of OPZ-SE from 28 to 21 and had a similar, but less substantial effect, on the phagocytosis of nonOPZ-SE. Lavage fluids collected after PI-3 virus inoculation, added to PI-3 virus-infected AM did not have a notable effect on the phagocytosis of OPZ-SE, but did cause a significant (P < 0.05) decrease in the percentage of phagocytosis of nonOPZ-SE from 25 to 17. The addition of virus-specific serum to infected AM caused significant (P < 0.05) decreases in the percentage of phagocytosis of OPZ-SE and nonOPZ-SE, with the values in the BHV-1-infected AM going from 28 to 11 and 16 to 9, respectively, and in the PI-3-infected AM from 36 to 12 and 25 to 13, respectively. Alveolar macrophages infected with either BHV-1 or PI-3 virus, in the presence or absence of lavage fluids from virus-infected calves or virus-specific serum, killed ingested SE as readily as noninfected AM. On the basis of the findings of this study, we suggest, as with other virus infections, that products of the host antiviral immune response interact with AM infected with BHV-1 or PI-3 virus or cause impaired internalization of receptor-bound particles, resulting in impaired AM antimicrobial functions.