The immune system is described as a network of cells, tissues, and organs that work together to assist the body’s ability to fight off diseases and infections. Infection occurs when microorganisms such as bacteria or viruses attack the body and proliferate in quantity. Therefore, the immune system normally fights these germs and prevents them from multiplying; thus, the immune system should be protected and healthy. When your immune response detects an antigen, it launches an attack. This is known as an immunological reaction. Antibodies are produced as part of this reaction. Antibodies are proteins that fight, neutralize, and kill antigens. The body produces more cells to resist the antigen. Following that, your immune response recalls the antigen. If it sees the antigen again, it will be able to recognize it. It will swiftly put out the appropriate antibodies, ensuring that you do not become ill in most cases. Immunity is the term used to describe this resistance against a certain disease.
Effects of stress on the immune system
Stress can impact the immune system since our immune system is inextricably linked to our stress levels. Because our brain and immune system constantly communicate with one another, physiological disturbances might manifest as physical symptoms. Stress impacts several immune activities, including reducing natural killer cell and T-cell cytotoxicity and compromising B-cell activity (King, 2018). Stress impairs our immune system’s ability to resist antigens, making us more vulnerable to infections due to our inability to fight the illness. Our bodies produce the stress hormone cortisol. Cortisol allows us to prepare our bodies to flee from the dangers we believe we are confronting. Cortisol accomplishes this by suppressing our immune system by reducing the quantity of protein needed to alert other immune cells (King, 2018). Common stressors have been linked to headaches, coronary heart disease, osteoporosis, arthritis, type 2 diabetes, chronic obstructive pulmonary disease, other aging-related disorders, and several malignancies.
The immune and stress systems are linked by various players, including interleukins, cytokines, and hormones. This connection between these systems may be crucial in the pathophysiology of various illnesses, including severe depression and illness. Proinflammatory cytokines, which operate on the vagus nerve or the BBB (amongst many other pathways), can stimulate the brain to change neural sensitivity to the social environment, resulting in increased sensitivity to social threat and social attachment. According to (Levy et al. (2018), upregulated proinflammatory mechanisms contribute to the risk of inflammatory disorders such as asthma, psoriatic arthritis, coronary heart disease, chronic pain, metabolic disorders, and possibly some cancers.
Moreover, when stress occurs, the connection between the brain and the body is impacted. Cytokine stimulation of the brain causes “ill behavior,” nervousness, and behavioral inhibition to decrease activity until healing occurs; fever and hunger suppression, as well as an associated drop in blood iron, stops viruses from replicating, thus not allowing the viruses and other germs to multiply as the immune system will have less or no information on any attack on the body.
When psychological stress occurs, it causes peripheral inflammation, which activates the occurrence of depression, psychosis, and bipolar disorder with microglial activation. When all these occur, the patient body resists any treatment, severe symptoms, and suicide overcome the immune system as the brain is affected thus does not send the right information and signal, weakening the body system. A wide variety of stress-producing events can increase susceptibility to illness. For instance, students in universities are more likely to develop acute infections and immune problems due to stress and anxiety due to exams; this may last for almost a month and thus trigger various illnesses such as headaches and other sorts of sickness.
Pathophysiological factors associated with depression.
Depression can also be triggered by chronic exposure to stress hormones, which reduce dopamine levels (Dallé & Mabandla, 2018). It is critical to recognize that some situations can cause stress and depression in almost any person. Most people recover from stress or depression within a few weeks or months, while some do not. Ways that stress can lead to depression include the following: • Prior or lengthy stresses might raise an individual’s odds of acquiring depression later in life; for example, being born and raised in a violent or uncaring home may increase the risk of developing depression later down the line. • Events that have a negative impact on an individual’s self-esteem, such as the breakup of a strong relationship or marriage • Feelings of shame,’ for example, when they believe, they have failed to meet their own or others’ goals. When individuals experience these stresses causing depression, the brain functionality is affected and does not function in its normal state; when germs, virus, or any other body threats attack, the connection between the body immune system and the brain tends to be poor; thus, the brain does not send message to the immune system to fight the threats. This results in increased chances of becoming sick.
Depression is a potentially fatal condition that affects millions of individuals worldwide. It can affect anyone at any age, from childhood to old age, and has a high societal cost because it produces extreme anguish and disruption of life and can be lethal if left untreated. The psychopathological condition is characterized by a variety of symptoms, including a low or sad mood, anhedonia, and a lack of energy or exhaustion. Other frequently present symptoms include insomnia and psychomotor abnormalities, a sense of guilt, low self-esteem, suicidal impulses, and autonomic and gastrointestinal disorders. Depression is not a monolithic condition but rather a multifaceted phenomenon with numerous kinds and likely more than one origin.
Many components (biogenic amine deficiency, genetic, environmental, immunologic, endocrine factors, and neurogenesis) have indeed been described as pathways that provide unitary theories for the pathophysiology of depression (Dallé & Mabandla, 2018). Genetic factors causing depression as a result of stress are those that are inherited from one generation to another. They are associated with melancholic depression, psychotic depression, and bipolar disorder, which impact the immune system to fight off the germs attacking the body (Dallé & Mabandla, 2018). They involve a combination of various genes rather than a single gene involved. The risk of developing clinical depression would be about 45% if the parent were diagnosed with the illness.
On the other hand, when a person experiences stress, it affects the biogenic amines that regulate brain processes such as motion, personality, feelings, temperature, blood pressure, and endocrine secretion, ultimately leading to depression. 40% of depression is caused by environmental factors within the individual’s own environment. These results from the unfavorable environment the person experiences, thus triggering the occurrence of stress causing depression. For instance, a child who is in an environment where there is mistreatment and abuse is likely to develop stress which is a long time leads to depression. Once these occur, the brain functionality and comfortability are affected, thus acting slow on sending a message to the immune system once the body is under attack from any germs, viruses, or any physical threat which causes wounds or any harm.
Dallé, E., & Mabandla, M. V. (2018). Early life stress, depression, and Parkinson’s disease: a new approach. Molecular brain, 11(1), 1-13.
King, P. T. (2018). The role of the immune response in the pathogenesis of bronchiectasis. BioMed research international, 2018.
Levy, M. J., Boulle, F., Steinbusch, H. W., van den Hove, D. L., Kenis, G., & Lanfumey, L. (2018). Neurotrophic factors and neuroplasticity pathways in the pathophysiology and treatment of depression. Psychopharmacology, 235(8), 2195-2220.