LIVER AND ADIPOSE TISSUE INTERPLAY THROUGH THE UP-REGULATION OF THE TH17 PATHWAY

CARLA CHACKELEVICIUS; GIRAUDI PABLO; GAMBARO SABRINA ELIANA; PALMISANO S; TIRIBELLI CLAUDIO; ROSSO NATALIA

Roma

Encuentro; 49th Annual Meeting of the Italian Association for the Study of the Liver; 2016

Associazione Italiana per lo Studio del Fegato

Background and aims: Chronic inflammation plays a key rolein the progression of NAFLD/NASH. Morbid obesity is tightly associ-ated to NAFLD. Adipose tissue from obese subjects has higher CD4Th17 cell content than controls. Periostin, an end-product of thepathway, is a secretory protein recently involved in both in vitroand in vivo fibrogenesis. The aim of this study is to explore theTh17 pathway in human NAFLD.Methods: We prospectively included 14 morbidly obese sub-jects undergoing bariatric surgery (50% men, mean age of 43 years(19-60), mean BMI 46.5). We analyzed mRNA expression of theTh17 pathway (RORC, IL-17, IL-17RA) and Periostin (POSTN) in liverand visceral adipose tissue biopsies. Patients were divided accord-ing Brunt?s score of liver fibrosis F0 (n = 2), F1 (n = 5), F2 (n = 7). Datawas correlated with the expression of other markers involved ininflammation and fibrosis.Results: We found that adipose tissue of patients with F2 stageof liver fibrosis shows an overexpression of RORC (p < 0.05) andIL-17RA (p < 0.05) genes respect to F0 group whereas IL17 was over-expressed only in F1 (p < 0.001). Moreover, hepatic gene expressionof RORC (p < 0.05), IL17RA (p < 0.05) and Periostin (p < 0.05) washigher in the F1 and F2 group compared with the F0. No changeswere observed in IL17 hepatic gene expression. These results are inline with those observed for inflammation and fibrosis markers.Conclusions: IL17 appears to be involved in the pathogenesisof liver inflammation and progression to fibrosis. Adipose tissueplays a role as a source of IL17 conferring higher risk of NAFLD toobese patients. Our preliminary data, in line with other reportedstudies, suggests that liver Periostin could be involved in hepaticfibrogenesis.Acknowledgements:    ToU05SPFRA14    ?    FRA    2014    (CdAdd.19.12.2014)  and  FIF.  CMC  is  supported  by  MAE;  PJG  byFondazione   Umberto   Veronesi   and   SEG   by   Project   MIUR-Nutrizione297.