The Microbiota-Gut-Immune-Glia (MGIG) Axis in Major Depression
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The Microbiota-Gut-Immune-Glia (MGIG) Axis in Major Depression Leszek Rudzki 1,2
&
Michael Maes 3,4,5
Received: 5 March 2020 / Accepted: 28 May 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract There is robust evidence that major depression (MDD) is accompanied by a low-grade activation of the immune-inflammatory response system, which is involved in the pathophysiology of this disorder. It is also becoming apparent that glia cells are in reciprocal communication with neurons, orchestrate various neuromodulatory, homeostatic, metabolic, and immune mechanisms, and have a crucial role in neuroinflammatory mechanisms in MDD. Those cells mediate the central nervous system (CNS) response to systemic inflammation and psychological stress, but at the same time, they may be an origin of the inflammatory response in the CNS. The sources of activation of the inflammatory response in MDD are immense; however, in recent years, it is becoming increasingly evident that the gastrointestinal tract with gut-associated lymphoid tissue (GALT) and increased intestinal permeability to bacterial LPS and food-derived antigens contribute to activation of low-grade inflammatory response with subsequent psychiatric manifestations. Furthermore, an excessive permeability to gut-derived antigenic material may lead to subsequent autoimmunities which are also known to be comorbid with MDD. In this review, we discuss fascinating interactions between the gastrointestinal tract, increased intestinal permeability, intestinal microbiota, and glia-neuron cross talk, and their roles in the pathogenesis of the inflammatory hypothesis of MDD. To emphasize those crucial intercommunications for the brain functions, we propose the term of microbiota-gut-immune-glia (MGIG) axis. Keywords Depression . Leaky gut . Microbiota . Cytokines . Neuroimmunomodulation . Oxidative stress . Glia . Microglia . Astrocytes . LPS . Autoimmunity . Neurodegeneration
Introduction In recent years, there has been growing evidence regarding abnormal glial functions and quantity in various psychiatric disorders such as schizophrenia, bipolar disorder, attention deficit hyperactivity disorder (ADHD), anxiety disorders, dementia, and major depressive disorder (MDD) [1] (Fig. 1). It is becoming clear that glia abnormalities have a crucial role in the neuroinflammatory pathophysiology of those disorders.
* Leszek Rudzki [email protected] 1
The Charleston Centre, 49 Neilston Road, Paisley PA2 6LY, UK
2
Department of Psychiatry, Medical University of Bialystok, Białystok, Poland
3
Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand
4
Department of Psychiatry, Medical University of Plovdiv, Plovdiv, Bulgaria
5
IMPACT Strategic Research Center, Deakin University, Geelong, Australia
MDD is also accompanied by volumetric brain reduction and a decrease in metabolic activity mostly in the hippocampus and medial prefrontal cortex (mPFC), and it is becoming evident that those changes are not only due to neu
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