Involvement of CCL2 in Salivary Gland Response to Hyperosmolar Stress Related to Sjögren's Syndrome.

In primary Sjögren's syndrome (pSS) patients, salivary gland (SG) epithelial cells (SGECs) could be exposed to chronic hyperosmotic stress (HOS), consecutive to their destruction and deregulation, that exacerbates an inflammatory response. The aims of this study were to assess the mechanism accounting for C-C motif chemokine ligand 2 (CCL2) expression in an immortalized human salivary gland epithelial acinar cell line (NS-SV-AC) subjected to HOS, as well as the involvement of CCL2 in pSS. CCL2 mRNA and protein levels were determined via RT-qPCR and ELISA. Reporter plasmids and a promoter pull-down assay were used to identify transcription factors associated with CCL2 mRNA increase. Our data showed that HOS-induced CCL2 mRNA increase was independent of the nuclear factor of activated T-cells 5 (NFAT5) and nuclear factor-kappa B (NFkB) but involved Kruppel-like factor 5 (KLF5). CCL2 protein levels, quantified by enzyme-linked immunosorbent assay (ELISA) in sera samples from pSS patients, correlated with the European Alliance of Associations for Rheumatology's Sjogren's syndrome disease activity index (ESSDAI) score for systemic activity. In addition, CCL2 protein levels were higher in patients with biological activity, cutaneous manifestations, and ESSDAI score superior or equal to five. Our data suggest that chronic HOS could exacerbate pSS disease by contributing to the inflammatory process induced by the expression and secretion of CCL2.

[Delayed renal infectious aneurysm 3 months after cardiac surgery for a Streptococcus pyogenes infective endocarditis ; case report and literature review]. / Anévrysme rénal infectieux retardé, 3 mois après chirurgie cardiaque pour une endocardite infectieuse à Streptococcus pyogenes ; cas et revue de la littérature.

Infective endocarditis (IE) due to Streptococcus pyogenes (SP) (Group A Streptococcus) is uncommon and infectious renal artery aneurysm (IRAA) is an exceptional complication of IE, with few cases reported in the literature. We describe a case of SP native mitral valve IE in a 58-year-old man, presenting with large valve vegetations, abscess and severe regurgitation. Initial CT-angiography showed bilateral kidney and splenic infarcts. He underwent successful emergent bioprosthetic valve replacement. Antibiotic regimen consisted in linezolid and rifampicin for 8 weeks. Three months later, CT-angiography for feet gangrene revealed a 16mm aneurysm of the left intraparenchymal renal artery, which was occluded by coil-embolization. This case shows that an infectious aneurysm may develop several months after antibiotic treatment and emergent valve replacement for IE.