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Chapter 10 endnote 3, from How Emotions are Made: The Secret Life of the Brain by Lisa Feldman Barrett.
Some context is:

When you have too much cortisol in your blood for a long time, inflammation flares up.

Inflammation is caused by many different types of cells in the body. For example, cells in the sympathetic nervous system (SNS) release the neurotransmitters noradrenaline and adrenaline, which are received by cells with certain receptors (called Beta-adrenergic receptors). This enhances pro-inflammatory gene expression and cytokines.[1]

Inflammation is also linked to cells in the adrenal gland (atop the kidneys) which releases cortisol into the blood stream. The adrenal glands can be stimulated by the SNS, or by hormones released into the blood stream, via the hypothalamic-pituitary-adrenal (HPA) axis (part of the body's endocrine system). In the short term, HPA axis activation suppresses pro-inflammatory gene expression and cytokines. (Cytokines also activate the HPA axis, which in turn releases cortisol that suppresses cytokines, so the immune system does not go into overdrive.)

Chronic body misbudgeting (with too much cortisol circulating the blood) limits the ability of cortisol to suppress inflammation. This results in increased baseline levels of inflammatory gene expression in circulating immune cells and increased vulnerability to disease. Chronic misbudgeting also causes an upregulation of SNS reactivity.[2]

Cytokines from the body can cross into the brain via a number of different pathway, including the nerve that stretches from your abdomen to your brainstem, called the vagus nerve, which also carries sensations resulting from visceral changes and inflammation to your brain.

The interoceptive network and the motor cortex control peripheral inflammation via the SNS and HPA axis.[3][4]

It was recently discovered that the immune system extends into the brain.[5] Less is known about inflammation in the cental nervous system, but it's well established that glial cells, specifically microglia, secrete cytokines and are responsible for cell death.

Notes on the Notes

  1. Pongratz, Georg, and Rainer H. Straub. 2014. "The sympathetic nervous response in inflammation." Arthritis Research and Therapy 16 (6): 504.
  2. Eisenberger, Naomi I., and Steve W. Cole. 2012. "Social neuroscience and health: neurophysiological mechanisms linking social ties with physical health." Nature Neuroscience 15 (5): 669-674.
  3. Levinthal, David J., and Peter L. Strick. 2012. "The motor cortex communicates with the kidney." The Journal of Neuroscience 32 (19): 6726-6731.
  4. Dum, Richard P., David J. Levinthal, and Peter L. Strick. 2016. "Motor, cognitive, and affective areas of the cerebral cortex influence the adrenal medulla." Proceedings of the National Academy of Sciences 113 (35): 9922-9927.
  5. Louveau, Antoine, Igor Smirnov, Timothy J. Keyes, Jacob D. Eccles, Sherin J. Rouhani, J. David Peske, Noel C. Derecki, David Castle, James W. Mandell, and Kevin S. Lee. 2015. “Structural and Functional Features of Central Nervous System Lymphatic Vessels.” Nature 523: 337–341.