The Role of the Immune System in Creating Depression, Post-traumatic-Stress-Disorder, and Psychosis

Research examining the role of inflammation in mental illnesses such as psychosisPsychosis, major depression, post-traumatic stressStress disorder has exploded. Whether inflammation is a feature in all cases of psychosisPsychosis and depression or just some remains an open question. The case is made that inflammation, possibly induced by stressStress or through exposure to a pathogen, plays a causal role in both affect disorders and psychosisPsychosis. StressStress, which occurs after the formation of perineuronal netsPerineuronal nets, can induce inflammation which is associated with reduced dopaminergic tone in the striatum and manifests as depression. If a stressor and associated inflammation occur before the formation of perineuronal netsPerineuronal nets, then fast-spiking, parvalbuminParvalbumin-positive, GABA interneurons are compromised and control of dopamineDopamine release in the from neurons in the ventral tegmental areaVentral tegmental area (VTA) is lost which manifests as psychosisPsychosis. This chapter reviews the support for these axioms. Then interventions to reduce inflammation are considered. These interventions include inducing the brain’s anti-panic circuitry which increases T regulatory cellsT regulatory cell, which release the anti-inflammatory cytokines TGF-βand IL-10. Additional anti-inflammatory mechanisms include increasing vagal toneVagal tone, increasing exercise, ensuring adequate sleepSleep, avoiding obesityObesity, and dietary changes. In the discussion of an anti-inflammatory diet, the role of microbiota in contributing to systemic inflammation will be considered along with a brief review of short-chain fatty acids.