Current Issues of Pharmacy and Medical Sciences

Curr Issues Pharm Med Sci., Vol. 33, No. 2, 106-111

Anna Dworzanska¹, Malgorzata Strycharz-Dudziak²*, Jakub Dworzanski¹,
Agnieszka Stec³, Barbara Rajtar³, Bartlomiej Drop⁴, Malgorzata Polz-Dacewicz³

¹ Masovian Specialist Hospital, Radom, Poland
² Chair and Department of Conservative Dentistry with Endodontics, Medical University of Lublin, Poland
³ Department of Virology, Medical University of Lublin, Poland
⁴ Department of Information Technology and Medical Statistics, Medical University of Lublin, Poland

 10.2478/cipms-2020-0020

© 2020 Author(s). This is an open access article distributed under the Creative Commons Attribution-NonComercial-No Derivs licence (http://creativecommons.org/licenses/by-nc-nd/3.0/)

Abstract

Epstein-Barr virus-associated gastric carcinoma (EBVaGC) is the most common malignancy caused by EBV infection. Toll-like receptors (TLRs) as major components of innate immune system are crucial in the development of inflammatory processes and carcinogenesis. The aim of our study was to evaluate tissue and serum level of TLR9 in EBV-positive and EBV-negative gastric cancer patients. The study involved 30 EBV(+) and 30 EBV(-) patients. EBV DNA was detected in fresh frozen tumor tissue. In serum samples TLR9 level, transforming growth factor β (TGFβ), interleukin 10 (IL-10) and antibodies against EBV were detected using ELISA tests. TLR9 level was also measured in homogenate of tumour tissue. TLR9 level was statistically lower in EBV(+) patients both in serum and tissue, with statistically higher level in tissue than in serum. Lower level of TLR9 was accompanied by higher level of Epstein-Barr virus capsid antigen (EBVCA), Epstein-Barr virus nuclear antigen (EBNA) and early antigen (EA). A lower level of TLR9 was detected in patients with poorly differentiated cancer (G3) and greater lymph nodes involvement (N3-N4). Lower level of TLR9 in patients with EA may point to TLR9 role in reactivation of EBV infection.

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Keywords

gastric cancer, TLR9, EBV, IL-10, TGFβ.