Response Of M2 Macrophages In A Simulated Tumor Microenvironment To Infection With Vesicular Stomatitis Virus

ASU Author/Contributor (non-ASU co-authors, if there are any, appear on document)
Rebecca Fuller (Creator)
Appalachian State University (ASU )
Web Site:
Maryam Ahmed

Abstract: Vesicular Stomatitis Virus (VSV) is a good candidate for oncolytic therapy due to its ability to induce apoptosis in a number of different types of cells. VSV's effect on macrophages has not been studied in-depth. Here, the effects of infection with both wild type (rwt) VSV and matrix (M) protein mutant (rM51R-M) VSV on cytokine production and cell viability of M2 macrophages cultured alone and in co-culture with MDA-MB-231 breast cancer cells were studied. Infection with rM51R-M VSV induced an increase in pro-inflammatory cytokines IL-6 production in co-culture conditions and TNF-a by M2 macrophages cultured alone. Viability of M2 macrophages cultured alone decreased after infection with both types of VSV. In co-culture conditions, cell viability decreased after infection with rwt VSV and increased after infection with rM51R-M VSV. We also set out to determine whether the MDA-MB-231 breast cancer cells or THP-1 monocytes were better labeled with fluorescent dye. Cancer cells were more readily labeled than monocytes. Working concentrations of dye were tested but an adequate concentration was not determined. Our data suggests that rM5R-M VSV can both modulate M2 macrophage phenotypes to a more M1-like phenotype and kill breast cancer cells, making it a suitable candidate for oncolytic therapy.

Additional Information

Honors Project
Fuller, R. (2018). "Response Of M2 Macrophages In A Simulated Tumor Microenvironment To Infection With Vesicular Stomatitis Virus." Unpublished Honors Thesis. Appalachian State University, Boone, NC.
Language: English
Date: 2018
Vesicular Stomatitis Virus, Oncolytic virus, macrophages, metastatic cancer, breast cancer

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