PMID- 10665530
OWN - NLM
STAT- MEDLINE
DCOM- 20000328
LR  - 20190831
IS  - 0378-1135 (Print)
IS  - 0378-1135 (Linking)
VI  - 71
IP  - 1-2
DP  - 2000 Jan
TI  - Effects of porcine reproductive and respiratory syndrome virus (isolate tw91) on 
      porcine alveolar macrophages in vitro.
PG  - 9-25
AB  - 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.
FAU - Chiou, M T
AU  - Chiou MT
AD  - Graduate Institute of Veterinary Medicine, College of Agriculture, National 
      Taiwan University, Taipei, ROC.
FAU - Jeng, C R
AU  - Jeng CR
FAU - Chueh, L L
AU  - Chueh LL
FAU - Cheng, C H
AU  - Cheng CH
FAU - Pang, V F
AU  - Pang VF
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Vet Microbiol
JT  - Veterinary microbiology
JID - 7705469
RN  - 0 (Antigens, Viral)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 11062-77-4 (Superoxides)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Animals
MH  - Antigens, Viral/analysis
MH  - Cells, Cultured
MH  - Dinoprostone/metabolism
MH  - Female
MH  - Hydrogen Peroxide/metabolism
MH  - Macrophages, Alveolar/*virology
MH  - Male
MH  - Microscopy, Electron, Scanning/veterinary
MH  - Phagocytosis
MH  - Porcine Reproductive and Respiratory Syndrome/*pathology
MH  - Porcine respiratory and reproductive syndrome virus/*pathogenicity
MH  - Specific Pathogen-Free Organisms
MH  - Superoxides
MH  - Swine
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2000/02/09 09:00
MHDA- 2000/04/01 09:00
CRDT- 2000/02/09 09:00
PHST- 2000/02/09 09:00 [pubmed]
PHST- 2000/04/01 09:00 [medline]
PHST- 2000/02/09 09:00 [entrez]
AID - S0378-1135(99)00159-5 [pii]
AID - 10.1016/s0378-1135(99)00159-5 [doi]
PST - ppublish
SO  - Vet Microbiol. 2000 Jan;71(1-2):9-25. doi: 10.1016/s0378-1135(99)00159-5.