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Stress and Autoimmune Disease: the role of adrenocorticotropic hormone (ACTH)

Stress can be physical, emotional or psychological. Depending on the pressures you are facing it can have varying effects on your body. When stressful situations occur your body releases stress hormones that give you the ability to fight back to intensify your concentration and your reaction. This process is mediated by the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis is a system in which cells of the hypothalamus secrete corticotrophin-releasing factor (CRF) in response to stress. CRF travels via the superior hypophyseal artery to the anterior pituitary where it binds receptors and initiates the stimulation/release of adrenocorticotropic hormone (ACTH). When ACTH is released it travels through the blood stream to the adrenal glands where cortisol and adrenalin are released to provide negative feedback to the hypothalamus and pituitary. If the HPA axis is over-activated for extended periods of time this can ultimately cause health issues such as depression, heart disease and autoimmune disease.

Research exposing links between stress and autoimmune disease continues to be an area of interest. Studies have shown stress may lead to immune dysregulation or to altered or amplified cytokine production, resulting in atopic autoimmune disease or decreased host defense. During extended periods of stress, Th2 and Th1 cells undergo altered response patterns. For example, antigen presenting cells (APCs) production of interleukin IL-12 is suppressed by the release of catecholamines and corticoids, thereby reducing Th1-cellular immunity causing an increase in susceptibility to common cold viruses. Additionally, Th2 cells are activated because secreted corticoids increase the production of interleukins IL-4, IL-10 and IL-13. These factors lead to a Th1/Th2 imbalance in favor of a Th2 mediated humoral response, which can elicit increased susceptibility to inflammation, allergy or atopic autoimmune disease.

Products for stress and autoimmune research:
ACTH ELISA
Substance P ELISA
Beta-Endorphin ELISA
Th2 Markers/Assays

References:

Takizawa, N., Tanaka, S., Oe, S., Koike, T., Yoshida, T., Hirahara, Y., ... & Yamada, H. (2018). Involvement of DHH and GLI1 in adrenocortical autograft regeneration in rats. Scientific reports, 8(1), 14542.

Lu, J., Montgomery, B. K., Chatain, G. P., Bugarini, A., Zhang, Q., Wang, X., ... & Chittiboina, P. (2018). Corticotropin releasing hormone can selectively stimulate glucose uptake in corticotropinoma via glucose transporter 1. Molecular and cellular endocrinology, 470, 105-114

Wang, D., Cai, M., Wang, T., Zhao, G., Huang, J., Wang, H., ... & Wang, Y. (2018). Theanine supplementation prevents liver injury and heat shock response by normalizing hypothalamic-pituitaryadrenal axis hyperactivity in mice subjected to whole body heat stress. Journal of Functional Foods, 45, 181-189.

Takizawa, N., Tanaka, S., Oe, S., Koike, T., Yoshida, T., Hirahara, Y., ... & Yamada, H. (2018). Involvement of DHH and GLI1 in adrenocortical autograft regeneration in rats. Scientific reports, 8(1), 14542.
 
Lu, J., Montgomery, B. K., Chatain, G. P., Bugarini, A., Zhang, Q., Wang, X., ... & Chittiboina, P. (2018). Corticotropin releasing hormone can selectively stimulate glucose uptake in corticotropinoma via glucose transporter 1. Molecular and cellular endocrinology, 470, 105-114
 
Wang, D., Cai, M., Wang, T., Zhao, G., Huang, J., Wang, H., ... & Wang, Y. (2018). Theanine supplementation prevents liver injury and heat shock response by normalizing hypothalamic-pituitaryadrenal axis hyperactivity in mice subjected to whole body heat stress. Journal of Functional Foods, 45, 181-189.