Academic Journal

A loss of function mutation in SOCS2 results in increased inflammatory response of macrophages to TLR ligands and Staphylococcus aureus

التفاصيل البيبلوغرافية
العنوان: A loss of function mutation in SOCS2 results in increased inflammatory response of macrophages to TLR ligands and Staphylococcus aureus
المؤلفون: Laurence Guzylack-Piriou, Blandine Gausseres, Christian Tasca, Chervin Hassel, Guillaume Tabouret, Gilles Foucras
المصدر: Frontiers in Immunology, Vol 15 (2024)
بيانات النشر: Frontiers Media S.A., 2024.
سنة النشر: 2024
المجموعة: LCC:Immunologic diseases. Allergy
مصطلحات موضوعية: SOCS2, R96C mutation, inflammatory response, macrophages, mice, Immunologic diseases. Allergy, RC581-607
الوصف: IntroductionThe role of suppressor of cytokine signaling (SOCS)2 in anti-infective bacterial immunity has been poorly investigated compared to other members of the SOCS family.MethodsWe 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 TLR-ligands and Staphylococcus aureus was examined.Results and discussionConversely 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-α pro-inflammatory cytokines production was only seen when the SOCS2 expression was promoted by the culture of macrophages in the presence of GM-CSF. Furthermore, we showed that the SOCS2 point mutation 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-γ 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.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1664-3224
Relation: https://www.frontiersin.org/articles/10.3389/fimmu.2024.1397330/full; https://doaj.org/toc/1664-3224
DOI: 10.3389/fimmu.2024.1397330
URL الوصول: https://doaj.org/article/84b30155990e4ab092ce12c44bc5a516
رقم الانضمام: edsdoj.84b30155990e4ab092ce12c44bc5a516
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:16643224
DOI:10.3389/fimmu.2024.1397330