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Stress and the Immune Response

Stress and the Immune Response

Introduction

The understanding of the components of complement system has endured a radical change since its discovery. Cortisol overwhelms inflammation by stopping the production of histamine, which decreases the susceptibility of an organism to various diseases. The immune system partly relies on T-lymphocytes, which are responsible for reaction to interleukins via the cell pathways. Interleukins are proteins that influence the exchange of messages between cells (“Inflammatory Mediators,” 2014). Moreover, T-lymphocytes belong to the complement system, which controls immunity (“Complement System,” 2014). In normal conditions, infectious stimuli affect the selection of interleukins. When the interleukin finds the needed cell, it joins the cell’s receptor. This process starts a chain of indications in the cell that results in the cell’s reaction to the infection agent. Furthermore, cortisol interferes with these processes preventing T-cells from distinguishing some indications that also stop T-cells from growing. As a result, the cortisol production decreases the immune reaction.

PTSD and the Complement System

In their study, Hovhannisyan, Mkrtchyan, Sukiasian, and Boyajyan (2010) discovered the commonly reduced activity of the supplement C3 component among PTSD patients. Furthermore, the authors presumed that such result explains the weakening of the C component caused by its overuse. The positive correlation between the components C3H50 and CH50 as well as the absence of any interactions between other components confirmed the aforementioned assertion. Therefore, such changes in the complement cascade serve as the indicator of the inference of the inflammatory factor in the etiology of PTSD. Thus, Hovhannisyan, Mkrtchyan, Sukiasian, and Boyajyan’s study (2010) demonstrates that the alteration of the complement affects the inflammatory response. Moreover, PTSD is related to the functional problems of the complement system, which exposes the altered chains in this complement cascade.

Inflammatory Response and the Brain

The central nervous system (CNS) and the immune system are interconnected since the CNS can react to the similar signals (Maier & Watkin, 2012). Furthermore, cytokines are produced when microglia are activated. These processes are responsible for the inflammatory response, which also affect behavior negatively resulting in sickness or depression. Moreover, in case of the sensitization of microglia, both CNS and immune system respond hyperbolically and subsequently have a long-term effect. Thus, the inflammatory response also becomes lasting or exaggerated. This means that sickness behavior extends and intensifies as well. Moreover, infection can cause sensitivity. In fact, there are several components oof the nervous system that react to infection. However, inflammation is a result of the response of the immune system, and that is why it is a part of the defense mechanism against infections (“Inflammatory Response,” 2014). Additionally, two groups of proteins, cytokines and chemokines, cause inflammation. These proteins’ messengers alter the activity of a variety of cells in this region. Cytokine receptors in the vagus nerve, for example, allow communicating with the brain while chemokines can attract other cells. Together, they can modify blood vessels increasing blood flow. They cross into the brain regions where the barrier is frail, thus causing the production of soluble mediators in the epithelial cells (Maier & Watkin, 2012).

Conclusion

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To conclude, the response to a stressor leads to physiological changes with an aim to help the organism cope with it. In turn, the activation of the stress response results in the release of cortisol, which mobilizes immune cells via glucocorticoid receptors, thus affecting the function that controls the activity of the immune system. However, the potential effects of PTSD on the inflammatory response happen because of cortisol, which is decreased among the patients with this disease. Thus, cortisol is critical in the stress response: its low levels in the PTSD patients can lead to infections and chronic inflammation.

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