Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2000-3-28
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0378-1135
pubmed:author
pubmed:issnType
Print
pubmed:volume
71
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
9-25
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Effects of porcine reproductive and respiratory syndrome virus (isolate tw91) on porcine alveolar macrophages in vitro.
pubmed:affiliation
Graduate Institute of Veterinary Medicine, College of Agriculture, National Taiwan University, Taipei, ROC.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't