Neutralizing Interleukin-6 in Tumor-Bearing Mice Does Not Abrogate Behavioral Fatigue Induced by Lewis Lung Carcinoma

Authors

Kiersten Scott
Thien Trong Phan
A Phillip West
Cullen M Taniguchi
Robert Dantzer

Publication Date

1-24-2022

Journal

Behavioural Brain Research

Abstract

Tumor growth is associated with metabolic reprogramming of various organs including the liver. This metabolic reprogramming is responsible for the development of behavioral fatigue represented by decreased voluntary wheel running in a murine model of lung cancer. To determine whether interleukin (IL-)6 induced by the tumor is responsible for the metabolic reprogramming, mice injected with Lewis lung carcinoma cells in the flank were treated with an anti-mouse IL-6 monoclonal neutralizing antibody using a 2 × 2 factorial design (+/- tumor and +/- anti-IL-6 antibody). Endpoints were represented by behavioral, metabolic and immune phenotypes. Despite its ability to abrogate the increase in plasma levels of IL-6 that was apparent in tumor-bearing mice and decrease inflammatory signaling in the liver, immunoneutralization of IL-6 had no effect on voluntary wheel running and did not modify the tumor-induced alterations in hepatic gene expression of inflammatory cytokines and metabolic factors. These negative results indicate that IL-6 does not mediate the communication between tumor and host in mice implanted with Lewis lung carcinoma.

Keywords

Animals, Antibodies, Monoclonal, Antibodies, Neutralizing, Carcinoma, Lewis Lung, Disease Models, Animal, Inflammation, Interleukin-6, Liver, Male, Mice, Mice, Inbred C57BL, Motor Activity, Muscle Fatigue, Cancer, Lewis lung carcinoma, Mouse, Interleukin-6, Fatigue, Liver metabolism, Inflammation

DOI

10.1016/j.bbr.2021.113607

PMID

34571117

PMCID

PMC8578453

PubMedCentral® Posted Date

1-24-2023

PubMedCentral® Full Text Version

Author MSS

Published Open-Access

yes