Citation

Santos JC, Pyter LM. Front. Immunol. 2018; 9: e1195.

Affiliation

Departments of Psychiatry and Behavioral Health and Neuroscience, The Institute for Behavioral Medicine Research, Ohio State University Wexner Medical Center, Columbus, OH, United States.

Copyright

(Copyright © 2018, Frontiers Research Foundation)

DOI

10.3389/fimmu.2018.01195

PMID

29930550

PMCID

PMC6001368

Abstract

Behavioral comorbidities (depression, anxiety, fatigue, cognitive disturbances, and neuropathic pain) are prevalent in cancer patients and survivors. These mental and neurological health issues reduce quality-of-life, which is a significant societal concern given the increasing rates of long-term survival after various cancers. Hypothesized causes of behavioral comorbidities with cancer include tumor biology, stress associated with the cancer experience, and cancer treatments. A relatively recent leading mechanism by which these causes contribute to changes in neurobiology that underlie behavior is inflammation. Indeed, both basic and clinical research indicates that peripheral inflammation leads to central inflammation and behavioral changes in other illness contexts. Given the limitations of assessing neuroimmunology in clinical populations, this review primarily synthesizes evidence of neuroimmune and neuroinflammatory changes due to two components of cancer (tumor biology and cancer treatments) that are associated with altered affective-like or cognitive behaviors in rodents. Specifically, alterations in microglia, neuroinflammation, and immune trafficking to the brain are compiled in models of tumors, chemotherapy, and/or radiation. Evidence-based neuronal mechanisms by which these neuroimmune changes may lead to changes in behavior are proposed. Finally, converging evidence in clinical cancer populations is discussed.

Language: en

Keywords

cognition; cytokines; depression; neuroinflammation; neuropathic pain