Host Defense Mechanisms are ways in which the body protects itself from pathogens - referred to as 3 lines of defense
The first 2 lines of defense are nonspecific, the 3rd line of defense, the immune response, is very specific
Antibodies
Special proteins produced in response to foreign substances called antigens
Lines of Defense
First Line
Second Line
Third Line
Nonspecific host defense mechanisms
General mechanisms that serve to protect the body against many harmful substances
Innate resistance
Exact factors that produce innate resistance are not well understood
Other nonspecific host defense mechanisms
Mechanical and physical barriers to invasion
Chemical factors
Microbial antagonism
Fever
Inflammatory response
Phagocytic white blood cells
First Line of Defense
Skin and mucous membranes as physical barriers
Cellular and chemical factors (e.g. pH, temperature, perspiration, enzymes)
Microbial antagonism
Transferrin
Glycoprotein that increases in response to systemic bacterial infections, binds to iron to deprive pathogens of this vital nutrient
Fever
Stimulated by pyrogenic substances, augments host's defenses by stimulating leukocytes, reducing available free plasma iron, and inducing the production of IL-1
Interferons
Small antiviral proteins produced by virus-infected cells, prevent viruses from multiplying
ComplementSystem
Group of about 30 different proteins in normal blood plasma, interact in a stepwise manner known as the complement cascade, assist in the destruction of many different pathogens
Opsonization is a process by which phagocytosis is facilitated by the deposition of opsonins (e.g. antibodies or certain complement fragments) onto objects (e.g. pathogens)
Acute-Phase Proteins
Plasma proteins that increase rapidly in response to infection, inflammation, or tissue injury
Cytokines
Chemical mediators released from many different types of cells, enable cells to communicate within the immune system and between the immune system and other systems of the body, some are chemoattractants that recruit phagocytes
Inflammation
1. Increase in capillary diameter (vasodilation)
2. Increased capillary permeability allowing escape of plasma and proteins
3. Exit of leukocytes from capillaries and accumulation at site of injury
Inflammation
Localizes infection, prevents spread of microbial invaders, neutralizes toxins, aids tissue repair
Causes redness, heat, swelling, and pain
Sequence of Events in Inflammation
1. Tissue Injury
2. Vasodilation
3. Increased Permeability
4. Emigration of Leukocytes
5. Chemotaxis
6. Phagocytosis
Inflammatory Exudate
Accumulation of fluid, cells, and cellular debris at the inflammation site
Purulent Exudate
Thick, greenish-yellow exudate containing many live and dead leukocytes, also known as pus
Phagocytosis
Process by which phagocytic white blood cells (phagocytes) surround and engulf (ingest) foreign material
Coating of microbes with complement components, such as C3b, making them more easily phagocytosed due to the presence of complement receptors on phagocytic cells
Ingestion Phase of Phagocytosis
1. Attachment
2. Pseudopodia extend around bacterial cell
3. Pseudopodia fuse
4. Bacterial cell is within the phagocyte
Digestion Phase of Phagocytosis
1. Lysosome with digestive enzymes moves toward phagosome
2. Lysosome membrane fuses with phagosome membrane
3. Lysosome and phagosome become a single membrane-bound vesicle
4. Bacterial cell is digested within the phagolysosome
Mechanisms by which pathogens escape destruction by phagocytes include capsules, exoenzymes that kill phagocytes, and not being destroyed within the phagolysosome
Disorders and conditions that adversely affect phagocytic and inflammatory processes include leukopenia, defects in leukocyte motility and chemotaxis, and chronic granulomatous disease
Additional factors that can impair host defense mechanisms
Nutritionalstatus
Increased iron levels
Stress
Cancer and cancer chemotherapy
Genetic defects
Age
AIDS
Drugs (e.g. steroids)
Leukopenia
an abnormally
low number of circulating
leukocytes