Introduction: Health and Stress
It was interesting to learn was how stress can have a negative impact of the body, and how it evolved because of flight-fight response. Our bodies are intended to respond to our condition with an end goal to safeguard homeostasis. However it was new to me to learn that the Autonomic Nervous System (ANS) and the Hypothalamic-Pituitary-Adrenal (HPA) axis play a major role in responding to stress. Chronic stress can have detrimental effects on the body including decreased immune functions, atherosclerosis as well as bone demineralisation etc. We also learn that due to trauma such as cell damage or infection a cascade of processes take place which result to inflammation. Inflammation is essential because it is responsible to eliminate the tissue damage or pathogenic microbes, which attracts immune cells into cells and which results to granulation, and leads to tissue repair.
Question: How does chronic stress lead to compromised health?
Chronic stress is maladaptive and detrimental to organism’s health, if it is repeatedly activated. Chronic stimulation of the Sympathetic Nervous System (SNS) due to chronic stress, results to a stimulation of cardiovascular system. This leads to an increased blood pressure and vascular hypertrophy. The muscles responsible for constricting the vasculature thicken, resulting to elevated rested blood pressure. Chronic high blood pressure consequently forces the heart to function harder, and results to hypertrophy of the left ventricle. The end result leads to damaged arteries and plaque formation . Chronic stress can also result to a significantly elevated stress hormone, such as cortisol and glucacartinoids which suppress immunity and particularly affect the distribution of cytokine presence. Cytokines are communication molecules, which mainly produced by immune cells. T helper 1 (Th1) and T helper 2 (Th2) which are involved in cellular and humoral immunity respectively become primarily dysregulated during exposure to chronic stress. This results to slower wound healing, and slower recovery from surgery. In addition chronic stress can be particularly detrimental to the elderly. There is a steady loss of immune function due to ageing, and when this is coupled with chronic stress it can lead to elderly being less able to produce antibodies to vaccinations, and their immune system in less effective at responding to a viral or bacterial infection .
• Inflammatory response and chronic disease
MURAKAMI M, & HIRANO T. (2012). The molecular mechanisms of chronic inflammation development. Frontiers in Immunology. 3.
This article reviews the inflammatory the mechanisms and pathogenesis associated with inflammation. Inflammation acts as a host defence against infectious agents as well as injury, however it can result to pathophysiology of many chronic diseases. Interactions between cells of the innate and adaptive immune system, in addition to inflammatory mediators can contribute to acute and chronic inflammation. Common effectors mechanisms of the inflammatory system, such as the complement system and phagocytosis result to tissue injury, angiogenesis, oxidative stress and fibrosis of tissue. The article mentions atherosclerosis as an example of a disease which is mediated by various inflammatory mediators involving both the innate and adaptive immune system. Overall I believe this article makes a significant impact in the field of cellular pathology, as a greater understanding and knowledge of the inflammatory response will help scientists devise new strategies to predict disease susceptibility. Also this base of knowledge could aid in the development of new approaches to prevent and treat chronic diseases such as atherosclerosis .
• Pathophysiology of the inflammatory response
BRØCHNER, A. C., & TOFT, P. (2009). Pathophysiology of the systemic inflammatory response after major accidental trauma. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. 17, 1-10.
The article explores the pathophysiology of the inflammatory response to trauma. Local inflammatory response happens due to trauma of tissue. Local mediators, such as kinis and arachidonic acid metabolites, as well as histamine released from mast cells are all activated during the response. They have a short half life, however their effects are long lasting. Following trauma, the complement system is also activated. The article explains that the system is activated by three pathways, including the antigen-antibody complex, bacterial cell wall components as well as mannan binding lectin pathway. The activation results to components of the cascade system that are able to oponise pathogens, lyse bacteria attract neutophils as well as attract platelets at the site of trauma . I believe that overall this article produces an excellent literature with regards to how the inflammatory response reacts to trauma. It explains well the complex mechanisms involved during the inflammatory response, and I therefore believe that it makes a significant contribution to the clinical field of the inflammation response.
• Mechanisms of Phagocytosis
ADEREM A. (2003). Phagocytosis and the inflammatory response. The Journal of Infectious Diseases. 187, 340-5.
The article explores the mechanism pathways involved in phagocytosis. Phagocytosis is the first line of defence step in the triggering of the host defence, in addition to inflammation. It’s essential for the removal of vast amounts of senescent cells that that are no longer necessary, as well in tissue remodelling and embryonic development. Phagocytosis activated by Pathogen-Associated Molecular Patterns (PAMPS), which results to the activation NF-kB, which is responsible for the control of DNA, cytokine production and overall survival of the cell. In addition oposonins such as antibodies and C3b can aid phagocytosis by acting as attachment positions. The article further explains that engulfment of foreign bodies is supported by the actin-myosin contractile system .
Overall, I believe that this article has made a vital contribution in the understanding on phagocytosis, given its crucial role in the regulation of the immune response.
- HENRY JP, STEPHENS PM, & SANTISTEBAN GA. (1975). A model of psychosocial hypertension showing reversibility and progression of cardiovascular complications. Circulation Research. 36, 156-64.
- SCHNEIDERMAN, N., IRONSON, G. AND SIEGEL, S. D. (2005). Stress and Health: Psychological, Behavioral, and Biological Determinants. Annual Review of Clinical Psychology, 1(1), pp.607-628.
- MURAKAMI M, & HIRANO T. (2012). The molecular mechanisms of chronic inflammation development. Frontiers in Immunology. 3.
- BRØCHNER, A. C., & TOFT, P. (2009). Pathophysiology of the systemic inflammatory response after major accidental trauma. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. 17, 1-10.
- ADEREM A. (2003). Phagocytosis and the inflammatory response. The Journal of Infectious Diseases. 187, 340-5.