To verify the role of porcine reproductive and respiratory syndrome virus (PRRSV)
infection on pulmonary defense mechanisms, alterations in the viability, morphology, and various functions of porcine alveolar macrophages (AMs) were evaluated in vitro for 2-72 h after exposure to a Taiwan isolate, tw91, 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 throughout the study. When compared with a mock-infected group, AMs from the PRRSV-infected group had a significantly lower viability at 18-72 h post-
infection (HPI) as determined by
trypan blue dye exclusion. Also during this time period, the cells showed morphological changes, including rounding,
bleb formation, and
rupture. The phagocytic and microbicidal capacity of AMs against Candida albicans was significantly inhibited after 6 HPI. Although the total amount of
superoxide anion (O2-) and
hydrogen peroxide (H2O2) produced by the AMs was reduced after 18 and 12 HPI, respectively, the amount of production was enhanced in both
reactive oxygen species on a per viable cell basis after 12 HPI. In contrast, the level of bioactive
tumor necrosis factor alpha (
TNF-alpha) secretion, either total or on a per viable cell basis, was markedly reduced soon after PRRSV
infection, up to 36 HPI, followed by a rebound thereafter.
Prostaglandin E2 (
PGE2) production was enhanced, both in total and on a per viable cell basis, in the first 6 h of
infection, especially at 2 HPI. However, it became lower than that of the control after 36 HPI. The results indicated that PRRSV
infection could cause, directly and/or indirectly, not only death of AMs but also adverse alterations in their morphology and function, although some of the effects seemed to be reversible. Because AMs are crucial to the host against airborne pathogens, PRRSV
infection may potentially predispose pigs to secondary pulmonary
infections.