Crosstalk between the Neuroendocrine and Immune Systems in Chronic Inflammatory Systemic Diseases

Hormonal and neuronal pathways either support or inhibit the manifestation of chronic inflammatory systemic diseases before the onset of the disease. After the onset of the disease, hormones and neurotransmitters may stimulate or inhibit the disease. Hormones and neurotransmitters modulate the course of the disease after disease onset. Examples are: 1) cortisol inhibits systemic chronic inflammatory disease, and 2) stress stimulates systemic chronic inflammatory disease. The active immune system in systemic chronic inflammatory diseases competes with the brain and other organ systems for energy-rich fuels, which leads to several disease sequelae. Chronic disease sequelae are sickness behaviour/fatigue/depressive symptoms, sleep disturbances, anorexia and malnutrition, bone loss, muscle wasting and cachectic obesity, insulin resistance with hyperinsulinaemia (accompanied by resistance to insulin-like growth factor-1), dyslipidaemia, alterations in the steroid hormone axes, disturbances of the hypothalamic-pituitary- gonadal (HPG) axis, elevated sympathetic tone, hypertension and volume overload, decreased parasympathetic tone, inflammation-related anaemia, and circadian rhythms of the symptoms. Disease sequelae are inherent to the disease and must be consistently treated.