Modulation of Stat-1 in Human Macrophages Infected with Different Species of Intracellular Pathogenic Bacteria
The infection of human macrophages by pathogenic bacteria induces different signaling pathways depending on the type of cellular receptors involved in the microorganism entry and on their mechanism(s) of survival and replication in the host cell. It was reported that Stat proteins play an important...
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Language: | English |
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Wiley
2016-01-01
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Series: | Journal of Immunology Research |
Online Access: | http://dx.doi.org/10.1155/2016/5086928 |
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author | Giuditta Fiorella Schiavano Sabrina Dominici Laura Rinaldi Alfonsina Mariarosaria Cangiano Giorgio Brandi Mauro Magnani |
author_facet | Giuditta Fiorella Schiavano Sabrina Dominici Laura Rinaldi Alfonsina Mariarosaria Cangiano Giorgio Brandi Mauro Magnani |
author_sort | Giuditta Fiorella Schiavano |
collection | DOAJ |
description | The infection of human macrophages by pathogenic bacteria induces different signaling pathways depending on the type of cellular receptors involved in the microorganism entry and on their mechanism(s) of survival and replication in the host cell. It was reported that Stat proteins play an important role in this process. In the present study, we investigate the changes in Stat-1 activation (phosphorylation in p-tyr701) after uptake of two Gram-positive (Listeria monocytogenes and Staphylococcus aureus) and two Gram-negative bacteria (Salmonella typhimurium and Legionella pneumophila) characterized by their varying abilities to enter, survive, and replicate in human macrophages. Comparing the results obtained with Gram-negative and Gram-positive bacteria, Stat-1 activation in macrophages does not seem to be related to LPS content. The p-tyr701Stat-1 expression levels were found to be independent of the internalized bacterial number and IFN-γ release. On the contrary, Jak/Stat-1 pathway activation only occurs when an active infection has been established in the host macrophage, and it is plausible that the differences in the expression levels of p-tyr701Stat-1 could be due to different survival mechanisms or to differences in bacteria life cycles within macrophages. |
format | Article |
id | doaj-art-3aadbeea80d54685aa5eaf1282e043a3 |
institution | Kabale University |
issn | 2314-8861 2314-7156 |
language | English |
publishDate | 2016-01-01 |
publisher | Wiley |
record_format | Article |
series | Journal of Immunology Research |
spelling | doaj-art-3aadbeea80d54685aa5eaf1282e043a32025-02-03T01:07:04ZengWileyJournal of Immunology Research2314-88612314-71562016-01-01201610.1155/2016/50869285086928Modulation of Stat-1 in Human Macrophages Infected with Different Species of Intracellular Pathogenic BacteriaGiuditta Fiorella Schiavano0Sabrina Dominici1Laura Rinaldi2Alfonsina Mariarosaria Cangiano3Giorgio Brandi4Mauro Magnani5Department of Biomolecular Sciences, Section of Toxicological, Hygienic and Environmental Sciences, University of Urbino Carlo Bo, Via S. Chiara 27, 61029 Urbino, ItalyDepartment of Biomolecular Sciences, Section of Biochemistry and Molecular Biology, University of Urbino Carlo Bo, Via Saffi 2, 61029 Urbino, ItalyDepartment of Biomolecular Sciences, Section of Toxicological, Hygienic and Environmental Sciences, University of Urbino Carlo Bo, Via S. Chiara 27, 61029 Urbino, ItalyDepartment of Biomolecular Sciences, Section of Biochemistry and Molecular Biology, University of Urbino Carlo Bo, Via Saffi 2, 61029 Urbino, ItalyDepartment of Biomolecular Sciences, Section of Toxicological, Hygienic and Environmental Sciences, University of Urbino Carlo Bo, Via S. Chiara 27, 61029 Urbino, ItalyDepartment of Biomolecular Sciences, Section of Biochemistry and Molecular Biology, University of Urbino Carlo Bo, Via Saffi 2, 61029 Urbino, ItalyThe infection of human macrophages by pathogenic bacteria induces different signaling pathways depending on the type of cellular receptors involved in the microorganism entry and on their mechanism(s) of survival and replication in the host cell. It was reported that Stat proteins play an important role in this process. In the present study, we investigate the changes in Stat-1 activation (phosphorylation in p-tyr701) after uptake of two Gram-positive (Listeria monocytogenes and Staphylococcus aureus) and two Gram-negative bacteria (Salmonella typhimurium and Legionella pneumophila) characterized by their varying abilities to enter, survive, and replicate in human macrophages. Comparing the results obtained with Gram-negative and Gram-positive bacteria, Stat-1 activation in macrophages does not seem to be related to LPS content. The p-tyr701Stat-1 expression levels were found to be independent of the internalized bacterial number and IFN-γ release. On the contrary, Jak/Stat-1 pathway activation only occurs when an active infection has been established in the host macrophage, and it is plausible that the differences in the expression levels of p-tyr701Stat-1 could be due to different survival mechanisms or to differences in bacteria life cycles within macrophages.http://dx.doi.org/10.1155/2016/5086928 |
spellingShingle | Giuditta Fiorella Schiavano Sabrina Dominici Laura Rinaldi Alfonsina Mariarosaria Cangiano Giorgio Brandi Mauro Magnani Modulation of Stat-1 in Human Macrophages Infected with Different Species of Intracellular Pathogenic Bacteria Journal of Immunology Research |
title | Modulation of Stat-1 in Human Macrophages Infected with Different Species of Intracellular Pathogenic Bacteria |
title_full | Modulation of Stat-1 in Human Macrophages Infected with Different Species of Intracellular Pathogenic Bacteria |
title_fullStr | Modulation of Stat-1 in Human Macrophages Infected with Different Species of Intracellular Pathogenic Bacteria |
title_full_unstemmed | Modulation of Stat-1 in Human Macrophages Infected with Different Species of Intracellular Pathogenic Bacteria |
title_short | Modulation of Stat-1 in Human Macrophages Infected with Different Species of Intracellular Pathogenic Bacteria |
title_sort | modulation of stat 1 in human macrophages infected with different species of intracellular pathogenic bacteria |
url | http://dx.doi.org/10.1155/2016/5086928 |
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