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Microscopy-based Assays for High-throughput Screening of Host Factors Involved in Brucella Infection of Hela Cells
Published on: August 5, 2016
Osmotically sensitive Brucella in infected normal and immune macrophages
1Department of Microbiology, University of Tennessee Medical Units, Memphis, Tennessee 38103.
Infection and Immunity
|February 1, 1970
Summary
Immune guinea pig macrophages reduce Brucella suis growth and induce osmotically sensitive forms. This indicates an immune response mechanism against Brucella suis infection.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Brucella suis is an intracellular pathogen that infects macrophages.
- The host immune response plays a critical role in controlling Brucella suis infections.
Purpose of the Study:
- To investigate the behavior of Brucella suis within normal and immune guinea pig macrophages.
- To determine the role of serum and immune status in Brucella suis intracellular survival and morphology.
Main Methods:
- Tissue culture of guinea pig macrophages (normal and immune).
- Infection of macrophages with Brucella suis.
- Monitoring of bacterial growth and survival over 72 hours.
- Assessment of bacterial osmotic sensitivity using sucrose-containing medium.
Main Results:
- Brucella suis multiplied significantly in normal macrophages without inducing osmotically sensitive forms.
- In immune macrophages with normal serum, Brucella suis numbers decreased, and no multiplication occurred.
- Approximately 50% of surviving Brucella suis in immune macrophages became osmotically sensitive after 6 hours.
- Brucella suis in immune macrophages with antiserum against guinea pig serum showed reduced, but present, osmotically sensitive forms.
Conclusions:
- Immune guinea pig macrophages restrict Brucella suis multiplication and induce the formation of osmotically sensitive Brucella.
- The presence of normal guinea pig serum enhances the immune macrophage-mediated control of Brucella suis.
- Osmotic sensitivity in Brucella suis appears to be a marker of immune-mediated stress or adaptation within macrophages.
