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Expression of functions by normal sheep alveolar macrophages and their alteration by interaction with Mycoplasma
M Niang1, R F Rosenbusch, J Lopez-Virella
1Department of Microbiology, Immunology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Ames 50011, USA.
Abstract:
Normal sheep alveolar macrophages collected by bronchial lavage were exposed to live or heat-killed Mycoplasma ovipneumoniae organisms, and their capability to ingest Staphylococcus aureus and to elicit antibody-dependent cellular cytotoxicity against sensitized chicken red blood cells was tested. Controls consisted of non-infected macrophages in M199 medium. In addition, the effect of M. ovipneumoniae on expression of surface molecules on these sheep alveolar macrophages was determined. The percentage of S. aureus ingested by nontreated sheep alveolar macrophages 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 alveolar macrophages to a similar degree. About 78% and 45% of the normal sheep alveolar macrophages had IgG and complement receptors, respectively. Infection of these macrophages with M. ovipneumoniae decreased significantly the expression of IgG receptors but had no effects on complement 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 effective in inducing expression of both classes than killed mycoplasmas. The results, taken together, suggest that M. ovipneumoniae induced alterations in macrophage activities and this may be a contributing factor in the pathogenesis of respiratory disease induced by the organism.
Insights
Mycoplasma ovipneumoniae infection impairs sheep alveolar macrophage function, reducing bacterial ingestion and antibody-dependent cellular cytotoxicity. This organism alters macrophage surface molecule expression, potentially contributing to respiratory disease pathogenesis.
Area of Science:
- Immunology
- Veterinary Microbiology
- Cell Biology
Background:
- Sheep alveolar macrophages are crucial for respiratory tract immunity.
- Mycoplasma ovipneumoniae is a significant respiratory pathogen in sheep.
- Understanding host-pathogen interactions at the cellular level is vital for disease control.
Purpose of the Study:
- To investigate the impact of Mycoplasma ovipneumoniae on sheep alveolar macrophage functions.
- To determine how M. ovipneumoniae affects the expression of surface molecules on macrophages.
- To elucidate the role of these alterations in the pathogenesis of ovine respiratory disease.
Main Methods:
- Sheep alveolar macrophages were exposed to live or heat-killed Mycoplasma ovipneumoniae.
- Macrophage phagocytic capacity for Staphylococcus aureus was assessed.
- Antibody-dependent cellular cytotoxicity against sensitized chicken red blood cells was measured.
- Expression of surface molecules (IgG receptors, complement receptors, MHC class I and II) was analyzed.
Main Results:
- M. ovipneumoniae infection significantly reduced Staphylococcus aureus ingestion by macrophages, with live organisms being more suppressive.
- Both live and killed M. ovipneumoniae suppressed antibody-dependent cellular cytotoxicity similarly.
- Infection decreased IgG receptor expression but did not affect complement receptors.
- M. ovipneumoniae increased the expression of MHC class I and II molecules, with live organisms being more potent inducers.
Conclusions:
- Mycoplasma ovipneumoniae significantly alters sheep alveolar macrophage functions, including phagocytosis and cytotoxicity.
- The organism modulates macrophage surface molecule expression, notably downregulating IgG receptors and upregulating MHC class I and II.
- These M. ovipneumoniae-induced macrophage alterations are implicated as a contributing factor in the pathogenesis of ovine respiratory disease.