S100B Up-Regulates Macrophage Production of IL1beta and CCL22 and Influences Severity of Retinal Inflammation

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Etat: Public
Version: Final published version
Licence: CC BY 4.0
ID Serval
serval:BIB_7235548BE398
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
S100B Up-Regulates Macrophage Production of IL1beta and CCL22 and Influences Severity of Retinal Inflammation
Périodique
PLoS One
Auteur⸱e⸱s
Niven J., Hoare J., McGowan D., Devarajan G., Itohara S., Gannage M., Teismann P., Crane I.
ISSN
1932-6203 (Electronic)
ISSN-L
1932-6203
Statut éditorial
Publié
Date de publication
2015
Volume
10
Numéro
7
Pages
e0132688
Langue
anglais
Notes
Niven, Jennifer
Hoare, Joseph
McGowan, Debbie
Devarajan, Gayathri
Itohara, Shigeyoshi
Gannage, Monique
Teismann, Peter
Crane, Isabel
eng
Research Support, Non-U.S. Gov't
PLoS One. 2015 Jul 23;10(7):e0132688. doi: 10.1371/journal.pone.0132688. eCollection 2015.
Résumé
S100B is a Ca2+ binding protein and is typically associated with brain and CNS disorders. However, the role of S100B in an inflammatory situation is not clear. The aim of the study was to determine whether S100B is likely to influence inflammation through its effect on macrophages. A murine macrophage cell line (RAW 264.7) and primary bone marrow derived macrophages were used for in vitro studies and a model of retinal inflammatory disease in which pathogenesis is highly dependent on macrophage infiltration, Experimental Autoimmune Uveoretinitis, for in vitro study. Experimental Autoimmune Uveoretinitis is a model for the human disease posterior endogenous uveoretinitis, a potentially blinding condition, with an autoimmune aetiology, that mainly affects the working age group. To date the involvement of S100B in autoimmune uveoretinitis has not been investigated. Real-time PCR array analysis on RAW 246.7 cells indicated up-regulation of gene expression for various cytokines/chemokines in response to S100B, IL-1beta and CCL22 in particular and this was confirmed by real-time PCR. In addition flow cytometry and ELISA confirmed up-regulation of protein production in response to S100B for pro-IL-1beta and CCL22 respectively. This was the case for both RAW 264.7 cells and bone marrow derived macrophages. Induction of EAU with retinal antigen in mice in which S100B had been deleted resulted in a significantly reduced level of disease compared to wild-type mice, as determined by topical endoscopic fundus imaging and histology grading. Macrophage infiltration was also significantly reduced in S100B deleted mice. Real-time PCR analysis indicated that this was associated with reduction in CCL22 and IL-1beta in retinas from S100B knock-out mice. In conclusion S100B augments the inflammatory response in uveoretinitis and this is likely to be, at least in part, via a direct effect on macrophages.
Mots-clé
Animals, Cell Line, Chemokine CCL22/*genetics/metabolism, Disease Models, Animal, Gene Expression Regulation, Interleukin-1beta/*genetics/metabolism, Macrophages/*immunology/pathology, Mice, Mice, Knockout, Retinitis/*genetics/metabolism/pathology, S100 Calcium Binding Protein beta Subunit/genetics/*metabolism, Uveitis/*genetics/metabolism/pathology
Pubmed
Création de la notice
10/03/2022 10:43
Dernière modification de la notice
23/11/2022 7:12
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