Healthy Immune System And Consequences Of Its Imbalances

Immunity is vital in defending the body against infections. This role is taken by the immune system comprising of a complex cell, tissues, organs, and protein networks. According to Stephenson, (2017), the immune system keeps a record of each and every microbe it has ever encountered and defeated as a way of controlling a future encounter. Important the body keeps a healthy immune system which can ideally create barriers to stop infections from entering the body above fighting them once they enter the body. At times, people may not realize when their immunity is at the tip-top. However, whenever something begins to go astray that is when people realize. A healthy immune system's main purpose is to protect the body from viruses and bacteria. These are the common causes of illnesses and hence the immune system has the ability to recognize any alien cell entering the body and destroy it. A healthy immune system needs to be balanced. An imbalanced immune system is weak and increases the body's susceptibility to diseases and infections.

Vitally, immunity protects the host body from microbes and chemicals commonly found in the environment. This helps in preserving the body's integrity in repelling and destroying these environmental agents. The human immune system uses specialized cells to fight alien cells that are harmful to the body cells. Humans have three types of immunity namely innate, adaptive, and passive immunity. Firstly, innate immunity is the type of immunity that every person is born with. This immunity is natural and serves as general body protection. Adaptive immunity is acquired and often might take days to weeks for it to be established. This kind of immunity tends to be more specific on pathogens and often keeps a memory of past attacks. Commonly, adaptive immunity gets established after the body gets exposed to an antigen that can either be from a vaccine or a pathogen. Finally, passive immunity is developed by a person upon receiving immune system components. Therefore, passive immunity develops when a person is given antibodies to fight a given infection rather than the body producing its own antibodies. (Iwasaki and Medzhitov, 2015 p. 24).

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Adaptive immunity is very specific in its ability to recognize and respond to a wide variety of pathogens. That is the reason why this type of immunity has a greater strength compared to other types of immunity. However, adaptive immunity gets a lot of support from the innate immunity that slows down the growth of pathogens giving adaptive immunity time to respond, control, eliminate pathogens and also, sends alert signals to adaptive immunity cells. Pathogens use a small chemical group referred to as antigens which are easily recognized as aliens by the T and B lymphocyte receptors. Adaptive immunity has a great ability in a way that it can easily identify and respond to any pathogen. Importantly, adaptive immunity can develop up to 100 trillion receptors needed to recognize any oncoming pathogen (Iwasaki and Medzhitov, 2015 p. 14).

The initial exposure of a pathogen to the immune system leads to a primary adaptive response. Therefore, initial infections show severe symptoms since adaptive immunity is not effective. When a re-exposure of the same pathogen occurs a secondary adaptive response is initiated. Since it is stronger than the primary adaptive response, it manages to eliminate the pathogen before causing any significant damages to tissues hence symptoms do not manifest. That forms the basis of immune memory responsible for the protection of diseases caused by similar pathogens (Black and Slavich, 2016 p.63).

Stephenson, (2017) argues that for the adaptive immune system to work efficiently in maintaining health, several components collaborate:

1. The lymphatic system comprised of bone marrow, lymph nodes, thymus, and spleen. These are responsible for carrying water, oxygen, and food to cells as well as removing waste. Importantly, the thymus allows the maturation of T cells critical in the adaptive immunity;
2. Leukocytes comprising of T&B lymphocytes, phagocytes, basophils, and mast cells. Generally, these elements are responsible for body protection against foreign invaders;
3. Antigens and antibodies are responsible for the stimulation of immune responses upon exposure. Each antigen has unique epitopes that cause specific responses;
4. Immune complexes that actively induce dendritic cell maturation and also promote activation and regulation of phagocytes;
5. The complement cascade enhances antibody and phagocytic ability in tackling microbes and damaged cells and further causes inflammation of pathogens cell membranes.

Immediate hypersensitivity. This type of hypersensitivity reaction occurs when mast cell activation is induced by the secretion of IgE antibodies. As a result, the antigen exposure leads to Th2 cell priming hence releasing IL-4. The IL-4 produced changes B cells from producing IgM and starts producing IgE antibodies. The IgE antibodies are antigen-specific and therefore end up binding with both the mast cells and basophils causing antigen sensitization. The antigen re-exposure comes into contact with the sensitized cells resulting in the production of preformed mediators such as prostaglandins, histamine, and leukotriene that cause rampant bronchoconstriction and vasodilation (Brockow et al., 2016 p.42).

Here, antibodies are targeting antigens that appear on the cell surface prompting an immune response. The IgG or the IgM antibodies attach to the cell surface antigens in a given tissue causing a complement system activation that in turn causes cell degranulation. When the neutrophils get DE granulated and the membrane is damaged the whole cell is damaged. This can eventually lead to tissue damage (Galvão and Castells, 2015 p. 36).

This hypersensitivity is caused by antigen-antibody complexes. The IgG antibodies bind to the circulating antigens. This results in the formation of immune complexes often deposited on the tissue membranes where there is high blood infiltration such as the kidney. As a result, the complement cascade attracts neutrophils resulting in cell phagocytosis (Galvão and Castells, 2015 p. 36). This type of hypersensitivity occurs as a result of antigen contact with pre-sensitized T lymphocytes. A combination of pre-sensitized T cells and CD4 respond to the antigen-presenting cells by releasing inflammatory cytokines. The inflammatory factors may lead to edema, redness, and local swelling. Also, it may lead to mediated cytotoxicity (Galvão and Castells, 2015 p. 36).

Diabetes mellitus. Medically, Diabetes mellitus is classified as an autoimmune chronic disease that results from the destruction of pancreatic beta cells, otherwise known as the ‘islets of Langerhans. These cells are responsible for the production of insulin in the human body. Studies have shown that type IV hypersensitivity is responsible for the destruction of the pancreatic beta cells. This occurs when the allergens penetrate the skin and are then taken up by the Langerhans cell in the pancreas. These allergens then migrate to the lymph nodes promoting the formation of sensitized T- lymphocytes. The T-lymphocytes activate the production of macrophages and inflammatory reaction in the tissues. The reaction is responsible for the destruction of the Langerhans cells, which produce insulin. That explains the reason why the individual must depend on insulin because the Langerhans cells have been destroyed by the hypersensitivity reaction. (Kharroubi, and Darwish, 2015 p.64)

Hay fever (allergic rhinitis) is the inflammation of the mucus membranes caused by the introduction of allergens into these mucus membranes. The allergen may either be pollen, animal dander, or molds. The site of antigen exposure determines the clinical sign and symptoms. When the reaction occurs in the upper respiratory tract and conjunctiva, the individual will develop sneezing and conjunctivitis. This type of reaction normally occurs after immediate exposure to the allergen, thus categorized as a Type I hypersensitivity reaction.

For this patient, exposure to environmental allergens crosses the nasal mucosa and enters the underlying tissue. The allergen then meets the previously sensitized mast cells and IgE/Fc receptor complexes from the previous infection with a similar allergen leading to the degranulation of the mast cell, releasing Histamine. Histamine then binds to H1 receptors on the mucosal surfaces resulting in vasodilatation and increased vessel permeability, consequently leading to edema. This mucosal swelling is responsible for nasal congestion. Itching occurs due to histamine stimulating nerve endings by H1 dependent mechanism. Sneezing, running nose, and tearing result from the combined effect of histamine and other inflammatory mediators such as prostaglandins, kinins, and leukotrienes. (Rennie et al., 2016 p.22).

Antihistamine mode of action. Histamines are inflammatory mediators in hypersensitivity reactions. Antihistamines reduce the effects of histamines in the body through binding to the H1 receptors in the mucosa, thus preventing the already produced histamine from binding to the H1 receptors, consequently reducing the symptoms associated with hypersensitivity

Drowsiness is a common side effect for those that cross the blood-brain barrier. They antagonize the neurotransmitter effect of histamine on H1 receptors in the Hypothalamus. Also, they cause anticholinergic side effects such as dry eyes, papillary dilatation, dry mouth, and urinary retention, and hesitance.

References:

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