This article discusses the effects of stress on the immune response and how it can lead to PTSD. It covers the alterations of the complement system activation in PTSD patients, the relationship between inflammation processes and the brain, and the consequences of the inflamed brain. The article also explains how exposure to a traumatic event causes the alteration of HPA axis and the development of PTSD.
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Stress and the Immune Response1Stress and the Immune Response Laura Peña-DuvalANT 100 / Stress and the Human BodyOctober 3, 2016Professor Iteeshree Mohapatra
Stress and the Immune Response2Under the normal conditions, immune cells control the presence and spread of any antigen anddestroy dead cells and pathogens. If any pathogen penetrates the body, inflammatory mediators signalimmune cells about the danger providing vasodilatation and increasing the vascular permeability (i.e.,histamine released by basophils in the blood and mast cells in tissues), activate pain receptors (i.e.,prostaglandins), or regulate immune cells (i.e., cytokines). These changes increase the blood flow in theregion of injury stimulating inflammation. As a result, plasma proteins and phagocytes migrate into theregion of injured tissue. Plasma proteins (cascade of complement system) activate immune responsemarking cells for phagocytosis, promoting inflammation, and destroying bacteria cells. Cortisolregulates the interactions between cytokines and immune cells. For example, cortisol inhibits T-cellproliferation blocking the interaction between interleukins and T-cell receptors. In addition, cortisolsuppresses the inflammation inhibiting histamine release (Randall, 2011).PTSD and the Complement SystemThe study demonstrates that PTSD is associated with the alterations of the complement systemactivation. The analysis of the major complement components in the blood serum of PTSD patientsshowed the increased activity of classical complement pathway, decreased the activity of alternativecomplement and overactivation of the complement terminal pathway. In addition, the data revealed thattwo complement pathways are not interdependent whereas alternative pathway is inhibited on theinitial stage of activation. In general, the results confirm that the alteration of the complement systemand inflammatory components are involved in the PTSD pathogenesis. Furthermore, previous studieshave shown that patients with PTSD have increased the number of white blood cells, higher levels ofinflammatory interleukins (IL-1b, IL-6) and lower level of anti-inflammatory interleukins (IL-4).Complement is a complex cascade of proteins modifications (proteolysis) consisting of three pathways(classical, alternative and lectin) with a single terminal pathway providing antibodies response,
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