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Proinflammatory response induced by Newcastle disease virus in tumor and normal cells

Authors Ginting TE, Suryatenggara J, Christian S, Mathew G

Received 3 October 2016

Accepted for publication 28 December 2016

Published 3 March 2017 Volume 2017:6 Pages 21—30


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Faris Farassati

Teridah Ernala Ginting, Jeremiah Suryatenggara, Salomo Christian, George Mathew

Division of Immunology, Mochtar Riady Institute for Nanotechnology and Medical Science Group, University of Pelita Harapan, Tangerang, Indonesia

Purpose: To investigate the specific role of immune responses induced by lentogenic Newcastle disease virus (NDV) for its antitumor effect.
Materials and methods: NDV LaSota strain was used to infect the following human cells: non-small cell lung carcinoma (A549), glioblastoma (U87MG and T98G), mammary gland adenocarcinoma (MCF7 and MDA-MB-453), hepatocellular carcinoma (Huh7), transformed embryonic kidney cells (HEK293), primary monocytes, lung fibroblast (HF19), skin fibroblast (NB1RGB) and rat astroglia (RCR-1) at 0.001 multiplicity of infection. NDV-induced cytotoxicity and expression of proinflammatory cytokines were analyzed using 3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide assay and multiplex enzyme-linked immunosorbent assay, respectively.
Results: Tumor cells (A549, U87MG, T98G, Huh7, MDA-MB-453, and MCF7) showed viability of <44%, while normal cell lines HEK293, NB1RGB, and RCR-1 showed 84%, 73%, and 69% viability at 72 hours postinfection, respectively. Proinflammatory cytokine profiling showed that NDV mainly induced the secretion of interferon (IFN)-α, IFN-β, and IFN-λ in tumor cells and only IFN-λ in normal cells. In addition, NDV infection induced the production of interleukin (IL)-6 in most cells.
Conclusion: Our findings suggest a new perspective regarding the role of IFN-λ and IL-6 in the mechanism of tumor selectivity and oncolysis of NDV.

Keywords: Newcastle disease virus, oncolytic virus, interferons, cytokines

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