PMID- 9477481 OWN - NLM STAT- MEDLINE DCOM- 19980326 LR - 20190831 IS - 0165-2427 (Print) IS - 0165-2427 (Linking) VI - 59 IP - 3-4 DP - 1997 Nov TI - Effect of porcine reproductive and respiratory syndrome virus (PRRSV) (isolate ATCC VR-2385) infection on bactericidal activity of porcine pulmonary intravascular macrophages (PIMs): in vitro comparisons with pulmonary alveolar macrophages (PAMs). PG - 323-35 AB - Porcine pulmonary intravascular macrophages (PIMs) were recovered by in situ pulmonary vascular perfusion with 0.025% collagenase in saline from six 8-week old, crossbred pigs. Pulmonary alveolar macrophages (PAMs) were recovered by bronchoalveolar lavage from the same pigs for comparisons in each assay. The macrophages were exposed to PRRSV (ATCC VR-2385) in vitro for 24 h and infection was confirmed by an indirect immunofluorescence test or transmission electron microscopy. Viral particles tended to accumulate in the vesicles of the Golgi apparatus or endoplasmic reticulum. Bactericidal function assays were performed on the recovered macrophages to determine the effects of the virus on macrophage functions. In vitro PRRSV infection reduced the bactericidal ability of PIMs from 68.3% to 56.4% (P < 0.09), and PAMs from 69.3% to 61.0% (P > 0.1) at 24 h post-infection. The mean percentage of bacteria killed by macrophages after PRRSV infection was not significantly different among the treatment groups or between the treatment groups and non-infected controls based on colorimetric MTT bactericidal (Staphylococcus aureus) assay. PRRSV did not affect the ability of PIMs or PAMs to internalize opsonized 125I-iododeoxyuridine-labeled S. aureus (P > 0.05). PRRSV infection significantly decreased the production of superoxide anion (P < 0.01) by 67.0% in PIMs and by 69.4% in PAMs. PRRSV reduced the myeloperoxidase-H2O2-halide product (P < 0.01) by 36.5% for PIMs and by 48.1% for PAMs. The results suggest: (1) PIMs should be considered as an important replication site of PRRSV; (2) PRRSV may have a detrimental effect on both PIMs and PAMs; (3) loss of bactericidal function in PIMs may facilitate hematogenous bacterial infections. FAU - Thanawongnuwech, R AU - Thanawongnuwech R AD - Veterinary Diagnostic Laboratory, College of Veterinary Medicine, Iowa State University, Ames 50011, USA. FAU - Thacker, E L AU - Thacker EL FAU - Halbur, P G AU - Halbur PG LA - eng PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - Netherlands TA - Vet Immunol Immunopathol JT - Veterinary immunology and immunopathology JID - 8002006 RN - 0 (Antigens, Viral) RN - 11062-77-4 (Superoxides) RN - 9679TC07X4 (Iodine) RN - EC 1.11.1.7 (Peroxidase) SB - IM MH - Animals MH - Antigens, Viral/analysis MH - *Blood Bactericidal Activity MH - Cell Separation MH - Cells, Cultured MH - Colorimetry MH - Fluorescent Antibody Technique, Indirect MH - In Vitro Techniques MH - Iodine/metabolism MH - Macrophages, Alveolar/*physiology MH - Peroxidase/metabolism MH - Phagocytosis MH - Porcine respiratory and reproductive syndrome virus/*physiology/ultrastructure MH - Staphylococcus aureus/*immunology MH - Superoxides/metabolism MH - Swine EDAT- 1998/02/27 00:00 MHDA- 1998/02/27 00:01 CRDT- 1998/02/27 00:00 PHST- 1998/02/27 00:00 [pubmed] PHST- 1998/02/27 00:01 [medline] PHST- 1998/02/27 00:00 [entrez] AID - S0165-2427(97)00078-0 [pii] AID - 10.1016/s0165-2427(97)00078-0 [doi] PST - ppublish SO - Vet Immunol Immunopathol. 1997 Nov;59(3-4):323-35. doi: 10.1016/s0165-2427(97)00078-0.