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Infection of macrophage-like THP-1 cells with Mycobacterium avium results in a decrease in their ability to
R C Garcia1, E Banfi, M G Pittis
1Leukocyte Biology Unit, International Centre for Genetic Engineering and Biotechnology, Area Science Park, 34012 Trieste, Italy. garcia@icgeb.trieste.it
Infection and Immunity
|May 19, 2000
Summary
Mycobacterium avium infection reduces nucleolin phosphorylation in macrophages. This study identifies decreased 110-kDa phosphonucleolin as a key change during infection.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Host-pathogen interactions are crucial in infectious diseases.
- Macrophages play a key role in the innate immune response to Mycobacterium avium.
- Understanding host response mechanisms targeted by pathogens is essential.
Purpose of the Study:
- To investigate the phosphorylation patterns of macrophage-like cells infected with Mycobacterium avium.
- To identify potential host targets affected by M. avium infection.
- To elucidate changes in phosphoprotein synthesis during mycobacterial infection.
Main Methods:
- Macrophage-like cells were infected with Mycobacterium avium.
- Cytosolic and membrane fractions were analyzed for phosphoprotein synthesis using [gamma-(32)P]ATP.
- Phosphoproteins were separated and identified using SDS-PAGE and amino acid sequencing.
Main Results:
- A significant decrease in a 110-kDa phosphoprotein was observed in cytosolic fractions of M. avium-infected cells.
- This 110-kDa phosphoprotein was identified as phosphonucleolin.
- The reduction in nucleolin phosphorylation was specific to M. avium infection and not due to changes in protein levels.
Conclusions:
- Mycobacterium avium infection leads to decreased phosphorylation of nucleolin in macrophages.
- Reduced phosphonucleolin may represent a host response mechanism interfered with by M. avium.
- Further research is warranted to explore the functional consequences of nucleolin dephosphorylation in M. avium infection.