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Host Defenses

Date: 21. November 2017

Principles of Host Defenses
Host defenses are composed of two complementary, frequently interacting systems: (1) innate (nonspecific) defenses, which protect against microorganisms in general; and (2) acquired (specific) immunity, which protects against a particular microorganism. Innate immunity is resistance that exists prior to exposure to the microbe (antigen). Innate defenses can be classified into three major categories: (1) physical barriers, such as intact skin and mucous membranes; (2) phagocytic cells, such as neutrophils, macrophages, and natural killer cells; and (3) proteins, such as complement, lysozyme, and interferon.

Adaptive immunity results either from exposure to the organism (active immunity) or from receipt of preformed antibody made in another host (passive immunity). Passive adaptive immunity is a temporary protection against an organism and is acquired by receiving serum containing preformed antibodies from another person or animal. Active adaptive immunity is protection based on exposure to the organism in the form of overt disease, subclinical infection (i.e., an infection without symptoms), or a vaccine. This protection has a slower onset but longer duration than passive immunity.

 

Innate Immunity
Innate immunity is the inborn ability of body to defend again pathogen and viral diseases. In the start of second section educator explains the skin and mucosalsurfaces in detail with illustrations. Innate immunity can be seen to comprise four types of defensive barriers: anatomic, physiologic phagocytic, and inflammatory. Major Functions are Killing invading microbes and Activating adaptive immune processes. Skin and Mucous Membranes- Intact skin is the first line of defense against many organisms. Fatty acids secreted by sebaceous glands in the skin have antibacterial and antifungal activity. The low pH of the skin (between 3 and 5), which is due to these fatty acids, also has an antimicrobial effect. Mucous Membrane of the respiratory tract, which is lined with cilia and covered with mucus. Other protective mechanisms of the respiratory tract involve alveolar macrophages, lysozyme in tears and mucus, hairs in the nose, and the cough reflex, which prevents aspiration into the lungs.

The nonspecific protection in the gastrointestinal tract includes hydrolytic enzymes in saliva, acid in the stomach, and various degradative enzymes and macrophages in the small intestine. The vagina of adult women is protected by the low pH generated by lactobacilli that are part of the normal flora. Additional protection in the gastrointestinal tract and in the lower respiratory tract is provided by defensins. These are highly positively charged (cationic) peptides that create pores in the membranes of bacteria, which kills them. The bacteria of the normal flora of the skin, nasopharynx, colon, and vagina occupy these ecologic niches, preventing pathogens from multiplying in these sites.

 

Inflammation
Inflammatory Response- The presence of foreign bodies, such as bacteria, provokes a protective inflammatory response. This response is characterized by the clinical findings of redness, swelling, warmth, and pain at the site of infection. These signs are due to increased blood flow, increased capillary permeability, and the escape of fluid and cells into the tissue spaces. The increased permeability is due to several chemical mediators, of which histamine, prostaglandins, and leukotrienes are the most important. Complement components, C3a and C5a, also contribute to increased vascular permeability. Bradykinin is an important mediator of pain.

Neutrophils and macrophages, both of which are phagocytes, are an important part of the inflammatory response. Neutrophils predominate in acute pyogenic infections, whereas macrophages are more prevalent in chronic or granulomatous infections. Macrophages perform two functions: they are phagocytic and they produce two important “proinflammatorycytokines: tumor necrosis factor (TNF) and interleukin-1 (IL-1). The synthesis of IL-1 from its inactive precursor is mediated by proteolytic enzymes (caspases) in a cytoplasmic structure called an inflammasome.

Certain proteins, known collectively as the acute-phase response, are also produced early in inflammation, mainly by the liver. The best known of these are Creactive protein and mannose-binding protein, which bind to the surface of bacteria and enhance the activation of the alternative pathway of complement. Neutrophils and macrophages are attracted to the site of infection by small polypeptides called chemokines (chemo tactic cytokines). Chemokines are produced by tissue cells in the infected area, by local endothelial cells, and by resident neutrophils and macrophages. 

 

Phagocytosis
As part of the inflammatory response, bacteria are engulfed (phagocytized) by polymorphonuclear neutrophils (PMNs) and macrophages. PMNs make up approximately 60% of the leukocytes in the blood, and their numbers increase significantly during infection (leukocytosis). Although both PMNs and macrophages phagocytose bacteria, PMNs do not present antigen to helper T lymphocytes, whereas macrophages (and dendritic cells) do. The process of phagocytosis can be divided into three steps: Migration, Ingestion and Killing.

Migration of PMNs to the infection site is due to the production of chemokines, such as interleukin-8 and complement component C5a, at that location. The bacteria are ingested by the invagination of the PMN cell membrane around the bacteria to form a vacuole (phagosome). This engulfment is enhanced by the binding of immunoglobulin G (IgG) antibodies (opsonins) to the surface of the bacteria, a process called opsonization. The C3b component of complement enhances opsonization. (The outer cell membranes of both PMNs and macrophages have receptors both for the Fc portion of IgG and for C3b.) Even in the absence of antibody, the C3b component of complement, which can be generated by the “alternative” pathway, can opsonize.

The killing of the organism within the phagosome is a two-step process that consists of degranulation followed by production of hypochlorite ions, which are probably the most important microbicidal agents. In degranulation, the two types of granules in the cytoplasm of the neutrophil fuse with the phagosome, emptying their contents in the process.

 

Adaptive Immunity
Adaptive immunity results either from exposure to the organism (active immunity) or from receipt of preformed antibody made in another host (passive immunity). Passive adaptive immunity is a temporary protection against an organism and is acquired by receiving serum containing preformed antibodies from another person or animal. Passive immunization occurs normally in the form of immunoglobulins passed through the placenta (IgG) or breast milk (IgA) from mother to child.

Fever- Infection causes a rise in the body temperature that is attributed to endogenous pyrogen (IL-1) released from macrophages. Fever may be a protective response because a variety of bacteria and viruses grow more slowly at elevated temperatures.

Passive Adaptive Immunity- Temporary protection against an organism and is acquired by receiving serum containing preformed antibodies from another person or animal. Passive immunization occurs normally in the form of immunoglobulins passed through the placenta (IgG) or breast milk (IgA) from mother to child. Passive immunity has the important advantage that its protective abilities are present immediately, whereas active immunity has a delay. Passive immunity has the important disadvantage that the antibody concentration decreases fairly rapidly as the proteins are degraded, and so the protection usually lasts for only a month or two

Active Adaptive Immunity -  Protection based on exposure to the organism in the form of overt disease, subclinical infection (i.e., an infection without symptoms), or a vaccine. This protection has a slower onset but longer duration than passive immunity. The primary response usually takes 7 to 10 days for the antibody to become detectable. An important advantage of active immunity is that an anamnestic (secondary) response occurs (i.e., there is a rapid response [approximately 3 days] of large amounts of antibody to an antigen that the immune system has previously encountered).

Afridi, Maham
  • Academics: MS 
  • Specialization: Medical Genetics
  • Current: Research Scholar 
  • University: Quaid-e-Azam University
  • Location: Islamabad, Pakistan
  •   
  • Course: Biochemistry 
  • Clinical Years: 2
  • Teaching Years: 1

Ms. Maham Afridi joined Quaid-e-Azam University as a research scholar in 2017, Before that she served in Core lab of National University Science and Technology Islamabad. She also served in Armed Forces Institute of Pathology in their department of Immunology, where her major roles were detection of antibodies and other immunology tests, genetic counselling etc.

Ms. Maham has full command on Genotyping of human genes, Risk assessment of genetic disorders, Diagnostic tests (TyphiDot, ELISA, Allergy tests), HPLC, PCR, Immunohistochemistry, Cell and tissue staining, Bacterial culturing, Cell culturing, DNA extraction, SDS PAGE, Gel Electrophoresis, Spectrophotometry.

Ms. Maham was awarded by Pak China Business forum in Recognition for poster presentation.

13 lectures