Immune Effects of M51R Vesicular Stomatitis Virus Treatment of Carcinomatosis From Colon Cancer.


Journal

The Journal of surgical research
ISSN: 1095-8673
Titre abrégé: J Surg Res
Pays: United States
ID NLM: 0376340

Informations de publication

Date de publication:
01 2020
Historique:
received: 30 03 2019
revised: 14 06 2019
accepted: 11 07 2019
pubmed: 16 8 2019
medline: 20 2 2020
entrez: 16 8 2019
Statut: ppublish

Résumé

The purpose of this study was to analyze the oncolytic and immunomodulatory functions of an M protein mutant of vesicular stomatitis virus (M51R VSV) in a murine model of peritoneal surface dissemination from colon cancer (PSD from CRC). Luciferase-expressing CT26 peritoneal tumors were established in Balb/c mice to evaluate the impact of M51R VSV treatment on intraperitoneal tumor growth and overall survival. The mice were treated with either intraperitoneal phosphate buffered saline (n = 10) or 5 × 10 A single, intraperitoneal treatment with M51R VSV inhibited the growth of PSD from CRC as evidenced by decreased bioluminescence and improved survival. This treatment approach also resulted in significantly higher frequencies of peritoneal CD4+ T (10.95 ± 1.17 versus 6.19 ± 0.44, P = 0.004) and B1b cells (5.01 ± 0.97 versus 2.20 ± 0.2, P = 0.024). On the other hand, treatment with M51R VSV resulted in fewer myeloid-derived suppressor cells relative to controls (10.66 ± 1.48 versus 14.47 ± 1.06, P = 0.035). M51R-treated peritoneal cavities also contained lower concentrations of immunosuppressive monocyte chemoattractant protein-1 and interleukin 6 cytokines relative to controls. Our findings suggest that M51R VSV alters the innate and adaptive immune responses in PSD from CRC. Future studies will delineate specific components of antitumor immunity that result in its therapeutic effect.

Sections du résumé

BACKGROUND
The purpose of this study was to analyze the oncolytic and immunomodulatory functions of an M protein mutant of vesicular stomatitis virus (M51R VSV) in a murine model of peritoneal surface dissemination from colon cancer (PSD from CRC).
METHODS
Luciferase-expressing CT26 peritoneal tumors were established in Balb/c mice to evaluate the impact of M51R VSV treatment on intraperitoneal tumor growth and overall survival. The mice were treated with either intraperitoneal phosphate buffered saline (n = 10) or 5 × 10
RESULTS
A single, intraperitoneal treatment with M51R VSV inhibited the growth of PSD from CRC as evidenced by decreased bioluminescence and improved survival. This treatment approach also resulted in significantly higher frequencies of peritoneal CD4+ T (10.95 ± 1.17 versus 6.19 ± 0.44, P = 0.004) and B1b cells (5.01 ± 0.97 versus 2.20 ± 0.2, P = 0.024). On the other hand, treatment with M51R VSV resulted in fewer myeloid-derived suppressor cells relative to controls (10.66 ± 1.48 versus 14.47 ± 1.06, P = 0.035). M51R-treated peritoneal cavities also contained lower concentrations of immunosuppressive monocyte chemoattractant protein-1 and interleukin 6 cytokines relative to controls.
CONCLUSIONS
Our findings suggest that M51R VSV alters the innate and adaptive immune responses in PSD from CRC. Future studies will delineate specific components of antitumor immunity that result in its therapeutic effect.

Identifiants

pubmed: 31415934
pii: S0022-4804(19)30527-X
doi: 10.1016/j.jss.2019.07.032
pii:
doi:

Substances chimiques

M protein, Vesicular stomatitis virus 0
Viral Matrix Proteins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

127-135

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

Auteurs

Gwenyth L Day (GL)

Department of Surgery, Wake Forest University School of Medicine, Winston-Salem, North Carolina.

Michelle L Bryan (ML)

Department of Surgery, Wake Forest University School of Medicine, Winston-Salem, North Carolina.

Scott A Northrup (SA)

Department of Surgery, Wake Forest University School of Medicine, Winston-Salem, North Carolina.

Douglas S Lyles (DS)

Department of Biochemistry, Wake Forest University School of Medicine, Winston-Salem, North Carolina.

Marlena M Westcott (MM)

Department of Microbiology and Immunology, Wake Forest University School of Medicine, Winston-Salem, North Carolina.

John H Stewart (JH)

Department of Surgery, The University of Illinois, Chicago School of Medicine, Chicago, Illinois. Electronic address: Jhstew4@uic.edu.

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Classifications MeSH