| Autor: |
Guzylack-Piriou, Laurence, Gausseres, Blandine, Tasca, Christian, Hassel, Chervin, Tabouret, Guillaume, Foucras, Gilles |
| Předmět: |
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| Zdroj: |
Frontiers in Immunology; 2024, p1-14, 14p |
| Abstrakt: |
Introduction: The role of suppressor of cytokine signaling (SOCS)2 in antiinfective bacterial immunity has been poorly investigated compared to other members of the SOCS family. Methods: We characterized the previously identified loss of function R96C point mutation of SOCS2 using a genome-edited mouse model that resumes the phenotype of Socs2 knockout mice. The response of macrophages to TLRligands and Staphylococcus aureus was examined. Results and discussion: Conversely to previously published data using human monocyte-derived macrophages, the stimulation of bone-marrow-derived macrophages with various TLR ligands did not show any difference according to the SOCS2 variant. Upregulation of IL-6 and TNF-a pro-inflammatory cytokines production was only seen when the SOCS2 expression was promoted by the culture ofmacrophages in the presence of GM-CSF. Furthermore, we showed that the SOCS2 pointmutation is associated with heightened STAT5 phosphorylation in a short time frame upon GM-CSF incubation. In mice, recruitment of neutrophil and F4/80int Ly6C+ inflammatory macrophage, as well as IFN-g and IL-10 concentrations, are significantly increased upon S. aureus peritoneal infection. Altogether, these data support the idea that by lowering the pro-inflammatory environment, SOCS2 favors better control of bacterial burden during a systemic infection caused by S. aureus. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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