3.6.4 Inflammation and immune response in psychiatric disorders

An Understanding of the Effects of Inflammation and the Immune Response on Neural Function

Numerous neuroanatomical, hormonal, and molecular channels are used by the CNS and immune system to communicate with one another. An intricate regulation mechanism necessary for good health is provided by the interplay between the neuroendocrine and immunological systems. Changes in autoimmune/inflammatory disease susceptibility and severity can result from disturbances at any level. A thorough understanding of the mechanisms by which the immune and CNS systems communicate at all levels will offer numerous new insights into the bidirectional regulation of these systems and the disruptions in these communications that cause disease, and ultimately will inform new therapeutic avenues for autoimmune/inflammatory diseases.

To avoid potentially harmful inflammation and preserve homeostasis, neural reflex circuits control cytokine release. The afferent vagus nerve carries sensory information triggered by injury or infection to integrative regions of the brainstem, and efferent nerves convey outbound impulses that terminate in the spleen and other tissues. Together, these signals form the inflammatory response. Following the release of acetylcholine from a fraction of CD4+ T cells, neurotransmitters from peripheral autonomic nerves carry the neurological signal to other immune cells, such as macrophages, by activating 7 nicotinic acetylcholine receptors.

In animal models of arthritis, alterations in the sympathetic nervous system and HPA axis during inflammation have been seen. More critically, these models have shown how crucial endogenous glucocorticoids are for controlling immunity and preventing mortality brought on by an unchecked immunological response. Furthermore, dysregulation of the Hypothalamic-Pituitary-adrenal (HPA), Hypothalamic-Pituitary-thyroid (HPT), Hypothalamic-Pituitary-gonadal (HPG), and GH axis is linked to rheumatoid arthritis (RA) in both humans and animals. Additionally, there is proof that the sympathetic nervous system struggles to control immunity and that glucocorticoid signalling is incorrect. Today, innovative RA treatments based on addressing and treating the dysregulation of these neurological and neuroendocrine circuits are being tested using these principles (Bauer & Teixeira, 2019).

Onset and Maintenance of Psychiatric Illness with Regards to Inflammation and Immune Response

Recent research reveals that inflammation may play a role in the symptoms of several psychiatric diseases, most notably depression. Numerous research, including meta-analyses, have linked depression to increased levels of acute phase proteins and peripheral and brain inflammatory cytokines. Chronically elevated inflammation is thought to alter neurotransmitters and neuro circuits, causing depressed symptoms and perhaps obstructing or reducing the effectiveness of antidepressants. In fact, studies have shown that people with high levels of inflammation respond poorly to standard antidepressant treatments. New avenues for the testing of novel treatment techniques that target the immune system or its impacts on neurotransmitter systems have been made possible by recent advancements in our capacity to comprehend and evaluate the effects of inflammation on the brain in patients (Alam et al., 2017).

The relationship between the immune system and psychiatric illness is complex and not fully understood. However, recent research suggests that immune responses may play a role in both the onset and maintenance of some psychiatric illnesses.

There is evidence that suggests that some psychiatric illnesses, such as depression and schizophrenia, may be related to an overactive or dysregulated immune response. This can result in inflammation in the brain, which has been associated with changes in neurotransmitter function and altered brain structure and function. In addition, there is evidence that suggests that some infections and chronic inflammation can trigger the onset of psychiatric illness. For example, individuals who have been infected with a virus or who have autoimmune conditions may be at increased risk for developing depression, anxiety, or other psychiatric illnesses.

There is also evidence that suggests that the immune system can play a role in the maintenance of psychiatric illness. For example, individuals with depression or schizophrenia may have chronic low-grade inflammation, which can contribute to the persistence of their symptoms.

Overall, while the relationship between the immune system and psychiatric illness is not fully understood, research suggests that immune responses may play a role in both the onset and maintenance of some psychiatric illnesses. As a result, targeting the immune system may provide a new avenue for the treatment of psychiatric illness.

References:

(1) Bauer, M. E., & Teixeira, A. L. (2019). Inflammation in psychiatric disorders: what comes first? Annals of the New York Academy of Sciences, 1437(1), 57-67.

(2) Alam, R., Abdolmaleky, H. M., & Zhou, J. R. (2017). Microbiome, inflammation, epigenetic alterations, and mental diseases. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, 174(6), 651-660.