EXPRESSION OF FUNCTIONS BY NORMAL SHEEP ALVEOLAR MACROPHAGES AND THEIR ALTERATION BY INTERACTION WITH MYCOPLASMA-OVIPNEUMONIAE

Citation
M. Niang et al., EXPRESSION OF FUNCTIONS BY NORMAL SHEEP ALVEOLAR MACROPHAGES AND THEIR ALTERATION BY INTERACTION WITH MYCOPLASMA-OVIPNEUMONIAE, Veterinary microbiology, 58(1), 1997, pp. 31-43
Citations number
31
Journal title
ISSN journal
03781135
Volume
58
Issue
1
Year of publication
1997
Pages
31 - 43
Database
ISI
SICI code
0378-1135(1997)58:1<31:EOFBNS>2.0.ZU;2-D
Abstract
Normal sheep alveolar macrophages collected by bronchial lavage were e xposed to live or heat-killed Mycoplasma ovipneumoniae organisms, and their capability to ingest Staphylococcus aureus and to elicit antibod y-dependent cellular cytotoxicity against sensitized chicken red blood cells was tested. Controls consisted of non-infected macrophages in M 199 medium. In addition, the effect of M. ovipneumoniae on expression of surface molecules on these sheep alveolar macrophages was determine d. The percentage of S. aureus ingested by nontreated sheep alveolar m acrophages was significantly higher than that of infected macrophages. Live mycoplasmas were more effective in suppressing the ingestion of S. aureus by these macrophages than killed mycoplasmas. Both live and killed mycoplasmas suppressed the cytolytic effect of the sheep alveol ar macrophages to a similar degree. About 78% and 45% of the normal sh eep alveolar macrophages had IgG and complement receptors, respectivel y. Infection of these macrophages with M. ovipneumoniae decreased sign ificantly the expression of IgG receptors but had no effects on comple ment receptors. There were substantial increases in the expression of both MHC class I and class II by the mycoplasma-induced macrophages as compared with unstimulated macrophages. Live mycoplasmas were more ef fective in inducing expression of both classes than killed mycoplasmas . The results, taken together, suggest that M. ovipneumoniae induced a lterations in macrophage activities and this may be a contributing fac tor in the pathogenesis of respiratory disease induced by the organism . (C) 1997 Elsevier Science B.V.