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Curr Top Behav Neurosci. 2017;31:73-94. doi: 10.1007/7854_2016_37.

Immune-to-Brain Communication Pathways in Inflammation-Associated Sickness and Depression.

Author information

1
Immunology Research Group, Calvin, Phoebe and Joan Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, 3280 Hospital Dr. NW, Calgary, AB, Canada, T2N 4N1.
2
Immunology Research Group, Calvin, Phoebe and Joan Snyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary, 3280 Hospital Dr. NW, Calgary, AB, Canada, T2N 4N1. swain@ucalgary.ca.

Abstract

A growing body of evidence now highlights a key role for inflammation in mediating sickness behaviors and depression. Systemic inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease, and chronic liver disease have high comorbidity with depression. How the periphery communicates with the brain to mediate changes in neurotransmission and thereby behavior is not completely understood. Traditional routes of communication between the periphery and the brain involve neural and humoral pathways with TNFα, IL-1β, and IL-6 being the three main cytokines that have primarily been implicated in mediating signaling via these pathways. However, in recent years communication via peripheral immune-cell-to-brain and the gut-microbiota-to-brain routes have received increasing attention for their ability to modulate brain function. In this chapter we discuss periphery-to-brain communication pathways and their potential role in mediating inflammation-associated sickness behaviors and depression.

KEYWORDS:

Cytokines; Depression; Gut microbiome; Microglia; Sickness behavior

PMID:
27677781
DOI:
10.1007/7854_2016_37
[Indexed for MEDLINE]

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