Activity 1

LOQUIAS, Hanna Kae F.

LOQUIAS, Hanna Kae F.

by Hanna Kae Loquias -
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ACTIVITY 1

Answer the following questions:

1. Briefly describe the process of inflammation in an area that has been traumatized.

As a biological immune system reaction to infections, injured cells, poisonous substances, or radiation, INFLAMMATION works to eliminate these harmful stimuli and start the healing process. An area of inflammation may exhibit PRISH: Pain (due to the release of certain chemicals); Redness (more blood is rushed to the affected area), Immobility (resulted from some loss of function in severe inflammations); Swelling (caused by an accumulation of fluids); and Heat (due to more blood rushed to the affected area) which are indications that an inflammatory response is being carried out in the body. Two classifications of Inflammation are acute or chronic. In acute inflammation the signs and symptoms develop rapidly and usually last for a few days or even a few weeks. In chronic inflammation, the signs and symptoms develop more slowly and can last for up to several months or years and are often severe.

The process of Inflammation occur in three basic stages:

STAGE 1: VASODILATION AND INCREASED BLOOD VESSEL PERMEABILITY

This first stage contributes to three of the signs and symptoms of inflammation: heat, redness (erythema), and swelling (edema). 

  1. Vasodilation (increase in the diameter) of arterioles

    • Vasodilation allows more blood to flow through the damaged area. The increased blood flow also helps remove microbial toxins and dead cells.      

    • Heat and redness result from the large amount of blood that accumulates in the damaged area. As the local temperature rises slightly, metabolic reactions proceed more rapidly and release additional heat.
  1. Increased permeability of capillaries 

    • substances normally retained in blood are permitted to pass from the blood vessels. 

    • permits defensive proteins such as antibodies and clotting factors to enter the injured area from the blood. 
    • Edema (Swelling) results from increased permeability of blood vessels, which permits more fluid to move from blood plasma into tissue spaces.

Substances that contribute to vasodilation and increased permeability: Histamine, Kinins, Prostaglandins (PGs), Leukotrienes, and Complement

STAGE 2: EMIGRATION OF PHAGOCYTES

Emigration 

  1. Neutrophils: 

    • After an hour of inflammatory process, phagocytes appear and neutrophils stick to blood vessel linings. They squeeze through vessels to reach damaged areas. 

    • This process depends on chemotaxis (stimulated movement of phagocytes to a site of damage)

    • Neutrophils destroy microbes through phagocytosis, while leukocytosis ensures a steady stream of neutrophils by increasing red blood cell production and release.
  1. Macrophages 

    • Neutrophils, primarily in early infection stages, die off rapidly. Monocytes follow neutrophils, transforming into wandering macrophages. 

    • True to their name, macrophages are much more potent phagocytes than neutrophils. These powerful phagocytes can engulf damaged tissue, worn-out neutrophils, and invading microbes.

  1. Pus 

    • Macrophages die, and a pocket of dead phagocytes and damaged tissue forms called pus.  

    • Pus formation occurs in most inflammatory responses and usually persists until the infection subsides. Sometimes pus reaches the body's surface or drains into an internal cavity, while other times it remains and is gradually destroyed and absorbed.

STAGE 3: TISSUE REPAIR

The tissue keeps remodeling, strengthening, and enhancing its cellular organization as it heals. Less new collagen is formed, but the collagen fibers are more organized and have stronger connections with one another.

 

 

2. Choose one type of Immunity (Innate and Humoral) and explain how its mechanism protects our body.

Since antibody-mediated immunity involves antibodies that bind to antigens in body humors or fluids, it is also referred to as humoral immunity. Humoral Immunity primarily involves the actions of B cells and the antibodies they produce to neutralize extracellular pathogens like bacteria and viruses. 

These is a breakdown of its mechanism:

  1. Antigen processing in a B cell: When an antigen is present, it is taken into the B cell, broken down into peptide fragments and combined with MHC-II self-antigens, and moved to the B cell plasma membrane. Helper T cells recognize the antigen–MHC-II complex and deliver the costimulation needed for B cell proliferation and differentiation. The helper T cell produces interleukin-2 and other cytokines that function as costimulators to activate B cells.

  2. Activation of B cells: In line with the presence of a foreign antigen, a specific B cell in a lymph node, the spleen, or mucosa-associated lymphatic tissue becomes activated. During activation of a B cell, an antigen binds to B-cell receptors (BCRs).

  3. Clonal selection: Then it forms a clone of plasma cells and memory cells. Plasma cells are the effector cells of a B cell clone which secrete specific antibodies, which in turn circulate in the lymph and blood to reach the site of invasion. On the other hand, memory B (long-lived) cells do not secrete antibodies. Instead, they can quickly proliferate and differentiate into more plasma cells and more memory B cells should the same antigen reappear at a future time. 

  4. Antibody defenses: Antibodies produced by a clone of plasma cells enter the circulation and form antigen–antibody complexes with the antigen that initiated their production. A few days after exposure to an antigen, a plasma cell secretes hundreds of millions of antibodies each day for about 4 or 5 days, until the plasma cell dies.

Antibodies (Ab), also known as immunoglobulins (Igs), are glycoproteins that can specifically bind to the epitope on the antigen that triggered their production. Most antibodies contain four polypeptide. Two of the chains are called heavy (H) chains and the other two are light (L) chains. There are five different classes, designated IgG (Protects from bacteria/viruses by enhancing phagocytosis), IgA (decreases during stress), IgM (Indicates the presence of a specific organism in a sick person), IgD (Involved in activation of B cells), and IgE (Involved in allergic and hypersensitivity reactions).

The immunoglobulin consists of Five Antibody Actions:

  1. Neutralizing Antigen - Blocks toxins which prevents attachment of some viruses to body cells.

  2. Immobilizing Bacteria - Antigen-antibody reaction inhibits motility to limit spread into tissues.

  3. Agglutinating and Precipitating Antigen - Antigen-antibody complex may cross link with other pathogens which results in agglutination or clumping. These are easily taken up by phagocytic cells. As a result, phagocytized precipitate will come out when attached to antibodies.

  4. Activating Complement - initiate the classical pathway of the complement system

  5. Enhancing Phagocytosis - serves as a flag/signal that attracts phagocytes.

Immune responses are much quicker and more intense after a second or subsequent exposure to an antigen than after the first exposure. This happens because of Immunological memory which is the presence of long-lasting antibodies and very long-lived lymphocytes that arise during clonal selection called memory B cells. One measure of immunological memory is antibody titer. These are the responses of our body to a specific antigen:

  1. Primary Response - After initial contact with an antigen, no antibodies are present for a period of several days. Then, a slow rise in the antibody titer occurs, first IgM and then IgG, followed by a gradual decline in antibody titer

  2. Secondary Response - Memory cells may remain for decades. Every new encounter with the same antigen results in a rapid proliferation of memory cells. After subsequent encounters, the antibody titer is far greater than during a primary response and consists mainly of IgG antibodies. 

Immunological memory is the foundation for vaccination against diseases like polio. Upon receiving the vaccine, B and T cells are activated, triggering a secondary response if the pathogen is encountered as an infecting microbe.

 

 

References: 

Tortora, G. J., & Derrickson, B. H. (2017). Principles of Anatomy and Physiology. (15th Ed.). John Wiley & Sons Inc.

Eng, C. (2023, July 15). The three stages of Inflamation.https://www.treloarphysio.com/the-three-stages-of-inflamation/

PubMed Central (PMC). (2018, Jan 23).  Inflammatory responses and inflammation-associated diseases in organs. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5805548/