Ch 16 Innate Host Defenses Flashcards
Adaptive defenses
Respond to particular agents called antigens. Adaptive defenses respond to these antigens by producing protein antibodies. Adaptive responses also involve the activation of the lymphocytes.
Antigens
molecules found in or on viruses and pathogenic bacteria that the body uses to identify them
Antibodies
Protein molecules created by the body to combat infection
Innate Defenses
Defenses of the body that act against any invading agent, not just a specific one. These defenses usually perform their function before the bodies adaptive defense mechanisms are activated. Innate defenses are however necessary to the activation of the adaptive defenses.
6 types of Innate immunity
- Physical Barriers
- Chemical Barriers
- Cellular defenses
- Inflammation
- Fever
- Molecular defenses
Physical Barriers
includes the skin, mucous membranes, and the chemicals that they secrete
Chemical Barriers
includes antimicrobial substances in body fluids such as saliva, mucus, gastric juices, and the iron limitation mechanisms
Cellular Defenses
consists of certain cells that engulf invading microorganisms (phagocytes)
Inflammation
the reddening, swelling, and temperature increases in tissues at sites of infection
Fever
the elevation of body temperature to kill invading agents and/or inactivate their toxic products
Molecular Defenses
interferon and complement, which destroy or impede invading microbes
Myeloid Stem Cells mature into
basophils, eosinophils, neutrophils, dendritic cells, and monocytes
Lymphoid Stem Cells mature into
B lymphocytes, T lymphocytes, and Natural Killer Cells
Granulocytes
have granular cytoplasm and an irregularly shaped, lobed nucleus. Include Basophis, Neutrophils, and eosinophils
Agranulocytes
Lack granular cytoplasm and have a round nucleus, Includes monocytes and lymphocytes
The process of Phagocytosis (4 steps)
Find (chemotaxis), adhere to, ingest, and digest
Phagocytosis: Chemotaxis (finding the cell)
In order to recognize invading microorganisms, Phagocytes use toll-like receptors (TLRs) that recognize molecular patterns unique to the pathogen, such as pepdidoglycan, lipopolysaccharide, flagellin, proteins, zymosan from yeast, and many other pathogen specific molecules. They are able to distinguish between gram + and gram - as well as bacterial and viral in order to tailor the response. During this process cytokines are released, which cause the attraction of more macrophages (chemokinees) and even inflammation.
Phagocytosis: Adherence
The ability of the phagocyte cell membrane to bind to specific molecules on the surface of the microbe, During this process the microbe can be coated with antibodies or with proteins of the complement system in order to make adherence much easier
Phagocytosis: Ingestion
here, the phagocyte forms fingerlike extensions called pseudophilia, that surround the microbe. These extensions then fuse and engulf the microbe within a cytoplasmic vacuole called a phagosome
Phagocytosis: Digestion
Phagocytic cells can digest microbes through several different methods. The first involves the lysosomes found within the phagocyte’s cytoplasm. These organelles fuse with the phagosome membrane creating a phagolysome. Digestive enzymes and densins are then released into the phagolysome and break down the microbe. Macrophages also can use other metabolic products to destroy ingested microbes. These include hydrogen peroxide, nitric acid, superoxide ions, and hypochloritic ions. Once the microbes are destroyed, indigestible material is left in the phagolysome, now called a resifual body, and transported into the plasma membrane where it is excreted.
Microbe Defence Mechanisms Against Digestion
- Interfering with chemotaxis
- antiphagocytic capsules
which make adherence
diffucult - Capsules that are invulnerable
to destruction by
macrophages, this allows the
microbe to reproduce within
the phagocyte - Some mirobes are just
naturally resistant to digestion
(mycobacterum & protozoa) - Other microbes produce
toxins that kill phagocytes
(leukocidins & streptolysin)
The lymphatic system
Provides many of the adaptive and innate defense mechanisms against infectious agents, collects excess fluid from the spaces between body cells, and transports digested fats to the cardiovascular system. Includes the lymph fluid, lymph nodes, and lymph vessels
B cells
mature in the bone marrow
T cells
mature in the thymus
The acute inflammatory process
Functions to (1) kill invading microbes (2) clear away tissue debris, and (3) repair injured tissue. Includes the use of histamine, vasodilation, edema, bradykinin, diapedesis, pus, fibroblasts, and granulation tissue
Histamine
When cells are damage, this is released from basophils and mast cells. It diffuses into nearby capillaries, causing the walls of these vessels to dilate and become more permeable.
Vasodilation
When the walls of vessels dilate and become more permeable. This increases the amount of blood flowing to the damaged area, which causes the skin around wounds to become red and warm to the touch.
Edema
Swelling. Because of vasodilation, the vessel walls are more permeable, fluids leave the blood and accumulate around the injured cells, causing edema
Bradykinin
Pain associated with tissue injury is thought to be due to the release of bradykinin, a small peptide, at the injured site. Cellular regulators called prostaglandins seem to intensify the effects.
Diapedesis
neutorphils pass out of the blood by squeezing between endothelial cells lining the vessel walls. This process allows neutrophils to congregate in tissue fluids at the injured regions.
Pus
The accumulation of dead phagocytes, injured or damaged cells, the remains of ingested organisms, and other tissue debris forms this white or yellow fluid
Fibroblasts
connective tissue cells that replace the destroyed tissue as a clot dissolves.
Granulation Tissue
new connective tissue and tiny blood vessels that form on the surfaces of a wound during the healing process.
Granulomatous Inflammation
Results in granulomas
Granuloma
a pocket of tissue that surrounds and walls off the inflammatory tissue. Helps to limit the spread of the infectious agent
Fever involves
exogenous and endogenous pyrogens
Exogenous Pyrogens
include exotoxins and endotoxins from infectious agents. These toxins cause fever by stimulating the release of an endogenous pyrogen from macrophages
Endogenous Pyrogens
a cytokine called interleukin-1 that circulates via the blood to the hypothalamus, where it causes certain neurons to secrete prostaglandins which reset the hypothalamus thermostat at a higher temp, causing the body temp to begin rising.
Beneficial roles of Fever
(1) raises body temp above optimum temp for growth of many pathogens
(2) At the higher temps of fever some microbial enzymes or toxins may be inactivated
(3) Fever can heighten the level of immune responses by increasing the rate of chemical reactions in the body.
(4) Phagocytosis is enhanced
(5) Production of antiviral interferon is increased
(6) Breakdown of lysosomes is heightened, causing death of infected cells and the microbes inside of them
(7) Causes the patient to feel ill, making it more likely that the patient rest, preventing any further damage and focusing energy on fighting the infection
Interferon
A small soluble protein that interferes with virus replication. There are three kinds that include alpha, beta, and gamma interferons.
Alpha & Beta Interferons
Seeing as the two are very similar, they have been placed together as type 1 interferons. The synthesis of these two interferons occurs after a virus infects a cell. They do not interfere directly with viral replication, but rather after viral infection, where the cell synthesizes and secretes minute amounts of interferon. They then diffuse to adjacent, uninfected cells and bind to their surfaces. This binding stimulates the production of certain mRNA that are transcribed into many new proteins. These are called Antiviral Proteins (AVPs). These proteins then interfere with viral replication once the virus infects the adjacent cells.
Gamma Interferons
Classified as type 2 interferons, these can also block virus replication via AVP synthesis, however they can be produced before viral infection in lymphocytes an NK cells that are sensitive to specific foreign antigens present in the body, Enhances activities of lymphocytes, NK cells, and macrophages. Also enhancces adaptive immunity by increasing antigen presentation. Also helps infected macrophages rid themselves of pathogens.
The complement System and Opsonization
Opsonization counteracts microbe defenses that prevent phagocytes from adhering to them. This starts when special antibodies called opsonins bind to and coat the surface of the microbe. The complement cascade is then initiated ultimately resulting in C3b binding to the surface of the microbe. Complement receptors on the plasma membrane of phagocytes recognize the C3b and this stimulates phagocytosis
The Complement System and Inflammation
C3a, C4a, and C5a enhance the acute inflammatory reaction by stimulating chemotaxis and thus phagocytosis. They also adhere to the membranes of basophils and mast cells causing them to release histamine
The Complement System and Membrane Attack Complexes
Another defense triggered by C3b is cell lysis. By a process called immune cytolysis, complement proteins produce lesions in cell membranes of microorganisms and other types of cells. These lesions cause cellular content to leak out The pore that is formed constitutes the Membrane Attack Complex (MAC) which is composed of the c5b, C6, C7, C8, and C9 proteins
Acute Phase Proteins
C-Reactive Protein and Mannose Binding Protein are produced during acute illness. These proteins can bind to the infectious agent and activate the complement cascade, as well as attract macrophages.
