Effects of porcine reproductive and respiratory syndrome virus (isolate tw91) on porcine alveolar macrophages in vitro

To verify the role of porcine reproductive and respiratory syndrome virus ( PRRSV) infection on pulmonary defense mechanisms, alterations in the viabil ity, morphology, and various functions of porcine alveolar macrophages (AMs ) were evaluated in vitro for 2-72 h after exposure to a Taiwan isolate, tw 91, at a multiplicity of infection (MOI) of 0.1. A low but constant rate of infection, around 5%, was seen in AMs from the PRRSV-infected group throug hout the study. When compared with a mock-infected group, AMs from the PRRS V-infected group had a significantly lower viability at 18-72 h post-infect ion (HPI) as determined by trypan blue dye exclusion. Also during this time period, the cells showed morphological changes, including rounding, bleb f ormation, and rupture. The phagocytic and microbicidal capacity of AMs agai nst Candida albicans was significantly inhibited after 6 HPI. Although the total amount of superoxide anion (O-2(-)) and hydrogen peroxide (H2O2) prod uced by the AMs was reduced after 18 and 12 HPI, respectively, the amount o f production was enhanced in both reactive oxygen species on a per viable c ell basis after 12 HPI. In contrast, the level of bioactive tumor necrosis factor cu (TNF-a) secretion, either total or on a per viable cell basis, wa s markedly reduced soon after PRRSV infection, up to 36 HPI, followed by a rebound thereafter. Prostaglandin E-2 (PGE(2)) production was enhanced, bot h in total and on a per viable cell basis, in the first 6 h of infection, e specially at 2 HPI. However, it became lower than that of the control after 36 HPI. The results indicated that PRRSV infection could cause, directly a nd/or indirectly, not only death of AMs but also adverse alterations in the ir morphology and function, although some of the effects seemed to be rever sible. Because AMs are crucial to the host against airborne pathogens, PRRS V infection may potentially predispose pigs to secondary pulmonary infectio ns. (C) 2000 Elsevier Science B.V. All rights reserved.