Back
Acta Physiologica 2011; Volume 203, Supplement 686
Joint Congress of FEPS and Turkish Society of Physiological Sciences
9/3/2011-9/7/2011
Istanbul, Turkey
DIETARY AFLATOXINS AND HEPATITIS B VIRUS INFECTION WITH RESPECT TO HEPATOCELLULAR CARCINOMA AND INFLAMMATION
Abstract number: W14
Yazihan1 Nuray, Yurdaydin2 Cihan, Sirin3 Burcu, Belen3 Asli, Akcil1 Ethem, Cesaretli4 Yildirim, Uzunalimoglu5 Ozden
1Ankara University, Faculty of Medicine, Pathophysiology Department, Ankara, Turkey
2Ankara University, Faculty of Medicine, Gastroenterology Department, Ankara, Turkey
3Ankara University, Faculty of Medicine, Molecular Biology R&D Unit Ankara, Turkey
4Refik Saydam National Public Health Agency Ankara, Turkey
5Turkish Hepatology Foundation, Ankara, Turkey
Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide and has an extremely poor prognosis. The major risk factors are chronic infection with hepatitis B viruses(HBV) as well as dietary exposure to aflatoxins. Prospective epidemiological studies have shown that there is a synergic interaction between HBV and aflatoxins in terms of HCC risk. However, the biology underlying this interaction is not fully understood. Midkine has mitogenic, antiapoptotic function in cancerogenesis and is also one of the inflammatory mediators. In this study, we aimed to evaluate underlying mechanisms of role of HBV infection in liver immune responses to carcinogenic/toxic substance aflatoxin B1. HBV infected(Hep3B) and noninfected(HepG2) human hepatocellularcancer cells cocultured with monocytic cells(THP-1) and are exposed to aflatoxin B1 for 24 h. Inflammatory responses of each cells defined with NFkB activation, IkB, TNF-a, IL-10, IFN-g and midkine secretion levels. Toll Like Receptor (TLRs) expression levels are evaluated by western blot. Exposure to aflatoxin results in activation of NFkB. The activation was higher in HBV infected group. HBV infection inhibits IFN-g secretion responses to aflatoxin in hepatocytes. TLR expression increased in cocultured hepatocytes in normal and aflatoxin exposed group. We found an increased inflammatory response that could be associated with the hepatotoxic effects of aflatoxin B1 in hepatocytes and monocytes. The predisposition of HBV-infected hepatocytes to aflatoxin-induced inflammatory damage is higher than non-infected hepatocytes. HBV infection supresses immune responses via inhibiting IFN-g production in liver cells. The increase in midkine secretion might be one of the underlying mechanisms of HBV induced carcinogenesis in aflatoxin exposure.
This study was supported by Ankara University.
To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 203, Supplement 686 :W14