Mouse Anti-Human IL-17 Hybridoma [HIL-23]

Background: Spontaneous bacterial peritonitis (SBP) is a potentially lethal complication of ascites. The inflammatory response is very intense in case of SBP despite low concentration of bacteria in the ascitic fluid with IL-17A overproduced by intestinal Paneth cells and may have role in host immune defense and inflammatory response. Aims: To study the diagnostic performance of serum and ascitic fluid IL-17A as a marker of SBP and its correlation with renal function. Methods: 120 cirrhotic patients including 80 patients with HCV-induced cirrhotic ascites but not with SBP and 40 patients with HCV-induced cirrhotic ascites with SBP were recruited. Serum and ascitic fluid IL17A were measured before and after treatment. Results: The mean serum and ascitic fluid levels of IL-17 in cirrhotic patients with SBP were significantly higher than in patients with cirrhosis without SBP (p < 0.001). Also, we found significant decline in both serum and ascitic fluid IL17 levels with successful treatment of SBP (p < 0.001). The sensitivity and specificity of serum IL17 was 100 % when using 92 pg/mL as cutoff. Meanwhile, sensitivity and specificity of ascitic fluid IL-17were 100 % when using 132 pg/mL as cutoff. Conclusions: IL-17 could be used as a possible diagnostic biomarker for SBP especially in culture negative and non-neutrocytic SBP and in monitoring therapeutic response. Also, it was shown to be related to hepatic and renal functions deterioration. (C) 2020 Elsevier Masson SAS. All rights reserved.

T-helper cell type 17 (Th17) mediated inflammation is associated with various diseases including autoimmune encephalitis, inflammatory bowel disease and lung diseases such as chronic obstructive pulmonary disease and asthma. Differentiation into distinct T helper subtypes needs to be tightly regulated to ensure an immunological balance. As microRNAs (miRNAs) are critical regulators of signalling pathways, we aimed to identify specific miRNAs implicated in controlling Th17 differentiation. We were able to create a regulatory network model of murine T helper cell differentiation by combining Affymetrix mRNA and miRNA arrays and in silico analysis. In this model, the miR-212 similar to 132 and miR-182 similar to 183 clusters were significantly up-regulated upon Th17 differentiation, whereas the entire miR-106 similar to 363 cluster was down-regulated and predicted to target well-known Th17 cell differentiation pathways. In vitro transfection of miR-18b, miR-106a and miR-363-3p into primary murine Cd4(+) lymphocytes decreased expression of retinoid-related orphan receptor c (Rorc), Rora, Il17a and Il17f, and abolished secretion of Th17-mediated interleukin-17a (Il17a). Moreover, we demonstrated target site-specific regulation of the Th17 transcription factors Rora and nuclear factor of activated T cells (Nfat) 5 by miR-18b, miR-106a and miR-363-3p through luciferase reporter assays. Here, we provide evidence that miRNAs are involved in controlling the differentiation and function of T helper cells, offering useful tools to study and modify Th17-mediated inflammation.