INFLAMMATION: TYPES AND MEDICAL SIGNIFICANCE

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Inflammation, a non-specificimmunologicalresponse is the general response of the body to microbial invasion or tissue injury (e.g., wound or burns). It usually involves a complex series of immunological response (comprising both the humoural and cellular immunity) that help to ward-off the establishment of an infection and thus initiate the repair processes of the damaged tissues. Inflammatory response therefore is the localized tissue response to injury, body trauma or microbial invasion – which can be characterized by pain, redness, swelling (oedema) and hotness. Inflammation generally represents a complex series of immunological reactions that occur following the invasion of a host by antigens. It is an immunological reaction which is mainly geared towards provoking the immune system to recruit antigen destroying cells (e.g., antibodies and phagocytes) to the site of attack so that the infection or antigen could be effectively contained and eliminated from the body. Inflammation is a natural and nonspecific immune response that acts as a biological barrier and one which defends the host against the attack of pathogens or antigens. It involves the combination of both the humoural and cell-mediated immune response. Inflammatory response can be acute or chronic depending on the duration of the immunological response in the host.

Chronic inflammation is a protracted type of inflammation that last a longer time and may take a week or more. This type of inflammation is usually aggravated when the antigen or pathogen persist for a longer period than normal in the affected host. Some clinical conditions that cause chronic inflammation include: inflammatory bowel disease (IBD), asthma, inflammatory arthritis and periodontitis. In acute inflammation, inflammatory response occurs almost immediately after the entry of the pathogen. Acute inflammation is usually caused by dermatitis, acute bronchitis and sinusitis. Acute inflammatory reaction is usually characterized by an instantaneous neutralization of the antigen or pathogen through a sequence of chain reactions including: (1) increase in body temperature (which prevent the growth of the pathogenic microbe); (2) recruitment of phagocytes to the site of inflammation (to eat or engulf the pathogenic microbe); (3) formation of clot (to inhibit the spread of the pathogen in vivo) and; (4) increase in the capillary flow of blood to the affected site (a mechanism that attract antibodies to the site of infection). Though characterized by both localized and systemic responses; inflammatory response is normally accompanied with an altered pattern of blood flow, influx of phagocytes to sites of damage, the recruitment of other immune system cells, and removal of the invading pathogen and possibly healing of the damaged tissue.

Inflammation plays a critical role in the complement system because the entirety of the complement system is mainly geared towards the production of inflammatory reactions which facilitates the quick localization of pathogens or antigens so that their pathogenicity in vivo could be contained and the infective agent possibly eliminated by other components of the immune system.An inflammatory response is usually described by five (5) fundamental features which are (Figure 1): (1) redness (rubor), (2) swelling/oedema (tumour), (3) heat (calor),(4) pain(dolor) and (5) loss of function (functio laesa). Swelling, redness, pain and heat are the main clinical features or symptoms of an inflammatory reaction.The redness is due to increased blood flow to the area of injury. The swelling is due to increased extra-vascular fluid and the infiltration of phagocytes to the damaged area. The heat is usually due to the increased blood flow to the site of injury and the action of fever-inducing agents (i.e., pyrogens). The pain is caused by local tissue destruction and irritation of sensory nerve receptors. Loss of function may occur if a whole organ or tissue of the body is impaired.

Figure 1. The five characteristics of inflammation. Inflammation is defined as a biological process that protects the body from microbial infection and other antigens that penetrate the intact body. It helps the body by producing white blood cells and other immunological substances that halts the spread of the invading antigen. When the inflammation process starts, chemicals in the white blood cells are released into the blood and the affected tissues to protect the body. The chemicals increase blood flow to the infected or injured body areas, causing redness and warmth in those locations.  Photo courtesy: https://www.verywellhealth.com/signs-of-inflammation-4580526

Inflammatory response is produced by the combined effort of a variety of immune system cells; and these include the cytokines (e.g., interleukins, tumor necrosis factors and interferons), the complement system, antibodies, neutrophils, macrophages and lymphocytes (inclusive of B cells and T cells). These immune system cells work cooperatively, following pathogen invasion of the host, to localize and limit the spread of the antigen to other sites of the body. Inflammation has several biological functions in the body especially during immune response; and it is an essential part of all immunological response to antigens or pathogens especially the complement system which it activates to inhibit the pathological activities of pathogenic microbes. For example, the fever or hotness (i.e., calor) experience during inflammatory response help to prevent the growth of the bacterial pathogen that invaded the body. If the invading pathogen is allowed to grow, the organism will multiply and proliferate in the host, thereby bringing about full clinical conditions characteristic of its disease or infection. This way, inflammation could be seen to provide a more protective role than a destructive one in the affected individual. Inflammatory response (both chronic and acute inflammation) involves a series of reactions which are all geared towards restricting further damage of host cells as well as ensuring the destruction of the invading pathogen. These features that characterize inflammation include phagocyte migration to site of inflammation, vasodilation and increased permeability of the capillaries to mention a few.   

CHARACTERISTICS OF INFLAMMATION

VASODILATION

Vasodilation is simply the relaxation of blood vessels (e.g., the capillaries and the arteries) so that they can be made wider than normal for increased blood flow in the body. As vasodilation is taking place, the veins that drains or carry blood away becomes constricted (a process known as vasoconstriction) and this results to rubor (i.e., redness)  and calor (i.e., heat) at the inflamed site, thus limiting the growth of the pathogen and the possible spread of the infection or pathogen to unaffected parts of the body. It is noteworthy that increase in the body temperature of the host provokes inflammatory reactions that may stop microbial growth at the inflamed site as aforementioned. The increased blood flow to the inflamed site also carries along antibodies and other immune system cells that destroy the antigen and eliminates it from the body.   

INCREASED PERMEABILITY OF THE CAPILLARIES

Increase in the permeability of the capillaries at the inflamed body tissue is of tremendous significance in inflammatory reaction. And this is because the increased capillary permeability allows neutrophils and other microbe-destroying cells to quickly reach the site of infection. During inflammation, antigen destroying cells (e.g., antibodies and neutrophils) are recruited to the site of inflammation or infection in a rapid fashion. And this is because the increased vascular permeability of the capillaries allows an increased flow of blood containing antibody-secreting plasma cells to the site of infection or inflammation. Oedema or tissue swelling is common at the site of infection due to the increased permeability of the capillaries. 

PHAGOCYTIC MIGRATION

Phagocytes are bacteria-eating cells. They engulf pathogenic microbes that enter the body and mediate their destruction in vivo. The migration of phagocytes to the site of infection or inflammation is important for inflammatory reactions because phagocytes engulf the antigen and limits their spread in the body. The destroyed pathogen is often released to the surface of the body or skin as pus cells or boils which contain dead cells, fluids and other digested materials. Aside the phagocytes, the macrophages, leukocytes and neutrophils are also recruited to the site of infection to mediate immunological damage that is of benefit to the host especially as it has to do with the destruction and elimination of the invading pathogenic microbe from the body.   

REPAIR PHASE

Inflammatory reaction is not only characterized by the destruction of host tissues invaded by pathogens. This nonspecific immune response (i.e., inflammation) also triggers the repair of damaged tissues and restores the tissue to their normal/healthy state after the inflammatory reaction. The repair phase is often the last phase of inflammation; and this stage of tissue healing is critical because a continued tissue damage especially in chronic inflammation may lead to the loss of function of the affected tissue.

Further reading

William E.P (2003). Fundamental Immunology. 5th edition. Lippincott Williams and Wilkins Publishers, USA.

Stevens, Christine Dorresteyn (2010). Clinical immunology and serology. Third edition. F.A. Davis Company, Philadelphia.

Silverstein A.M (1999). The history of immunology. In Paul, WE (ed): Fundamental Immunology, 4th edition. Lippincott Williams and Wilkins, Philadelphia, USA.

Paul W.E (2014). Fundamental Immunology. Seventh edition. Lippincott Williams and Wilkins, USA.

Male D, Brostoff J, Roth D.B and Roitt I (2014). Immunology. Eight edition. Elsevier Saunders, USA.

Levinson W (2010). Review of Medical Microbiology and Immunology. Twelfth edition. The McGraw-Hill Companies, USA.

Berzofsky J.A and Berkower J.J (1999). Immunogenicity and antigen structure. In Fundamental Immunology, 4th edition., W.E. Paul, ed., Lippincott-Raven, Philadelphia. 

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