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Immunology Non-specific Host Defenses

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Immunology Non-specific Host Defenses Non-specific means that the defenses that are used to protect the body act the same no matter what the infection is. – PowerPoint PPT presentation

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Title: Immunology Non-specific Host Defenses


1
ImmunologyNon-specific Host Defenses
  • Non-specific means that the defenses that are
    used to protect the body act the same no matter
    what the infection is. Specific defenses are
    specific to the disease, such as antibodies made
    for each individual disease.

2
Nonspecific Host Defenses
  • Skin and mucous membranes provide a mechanical
    barrier to keep organisms from entering the body.
    They work only if there are no cracks or tears,
    etc.
  • Additional aids to contribute to the defense
    provided by the skin and mucous membranes are
  • Lacrimal secretions (tears) wash dirt and germs
    from the eyes
  • Saliva washes food and germs off of the teeth
  • Mucous in RT and GIT traps dirt and germs so
    they cant colonize the membrane surface

3
  • Ciliated cells move mucous, dirt and germs out
    of the body
  • Urine washes dirt and germs out of the urethra
  • Vaginal secretions helps maintain normal pH,
    washes out dirt and germs
  • Chemical factors that aid in defense
  • Sebum oil made by glands of the skin, trap dirt
    and germs
  • Perspiration flush org. off skin and produce
    lysozyme (break down cell wall of G)
  • Gastric juice destroys most bacteria and toxins
    due to pH and acids

4
  • Normal Microbiota
  • Aid in preventing disease by
  • competing for attachment sites.
  • competing for nutrients.
  • making and excreting antimicrobials.
  • Genetics
  • Some host are genetcially resistant to infection
    by some organisms. For example, many diseases
    are specific to humans and do not infect animals,
    or vice versa.
  • Monkeypox infects monkeys but does not cause
    disease in humans

5
Nonspecific Defenses in the Blood
  • Phagocytes (White Blood Cells) 2nd line of
    defense.
  • Neutrophils first responder to the scene of the
    accident. Neutrophils begin cleaning up invading
    microorganisms by phagocytosis.
  • As the infection progresses, macrophages dominate
    the clean up process.
  • They begin as monocytes. Monocytes are not
    active phagocytes while in the blood. Once they
    move out of the blood vessels and into the
    infected tissue, they mature into macrophages,
    active phagocytes.

6
The process of phagocytosis
  • See Fig. 14.19
  • Recognition Pathogen recognized as foreign by
    phagocyte due to foreign proteins on the surface
    of the organism.
  • Proteins on the surface of cells are used as
    markers to identify the good guys and the bad
    guys. The bodys cells have markers that tell
    the immune system that they belong there and not
    to attack while the bad guys have foreign markers
    that are not recognized and signal the immune
    system that it doesnt belong there.
  • Adherence phagocyte binds to pathogen.
  • Ingestion pseudopods are extended around the
    pathogen and the pathogen is engulfed into a sac
    inside the cell. This is called a phagosome.

7
  • Digestion lysosomes within the cell migrate to
    the phagosome and merge with it, creating a
    phagolysosome. Chemicals that are toxic to the
    pathogen are released inside the phagolysosome
    leading to its digestion.
  • Release of Debris Once the pathogen has been
    digested into small particles, the cell releases
    the undigestible debris into the surrounding
    environment.

8
Inflammation
  • Triggered by damage to bodys tissues.
  • 5 signs and symptoms
  • Redness
  • Pain
  • Heat
  • Swelling
  • Sometimes loss of function

9
  • Purpose of Inflammation
  • Destroy injurious agent and remove it if
    possible.
  • Limit effects on body by walling off injurious
    agent and its by-products away from the rest of
    the body.
  • Repair tissue damaged by the injurious agent or
    its by-products.

10
  • 3 stages of Inflammation
  • Vasodilation and increased permeability of blood
    vessels
  • Increase in blood flow to help get the immune
    cells to the injured site more quickly and dilute
    toxic substances.
  • Allows defensive substances, such as phagocytes,
    to pass through the walls and enter the injured
    area.
  • Phagocyte Migration and Phagocytosis
  • Blood flow decreases, phagocytes begin to squeeze
    between endothelial cells to reach damaged area.
  • Phagocytes begin destroying invading
    microorganisms.

11
  • Tissue repair
  • Begins during inflammation but cannot be
    completed until all harmful substances have been
    removed or neutralized.
  • Fever
  • The benefits of fever as still being debated and
    proved.
  • It was thought as recently as 5-10 years ago that
    the increased body temperature killed invading
    microorganisms by providing an atmosphere that
    was too hot for them to survive.
  • That has since been shown to be mostly false.
    Most microorganisms require a much higher
    temperature change to be affected than that
    caused by a fever.

12
  • However, your textbook does mention a few
    organisms that seem to be sensitive to the small
    temperature change, such as the Polio virus and
    the Chickenpox virus.
  • There is some evidence that fever impedes the
    nutrition of bacteria by reducing the available
    iron.
  • And it increases metabolism and immune responses.
  • In general, whether or not slight to moderate
    fevers should be treated is still being debated.

13
Other Antimicrobial Substances In Blood
  • Complement and Interferon
  • Complement Has several different functions.
  • 20 different proteins found in normal serum.
  • Punch holes in membranes of pathogens, releasing
    cellular contents. Called the Membrane Attack
    Complex or MAC.
  • Contribute to development of inflammation.
  • Coat outside surface of pathogen which enhances
    phagocytosis.

14
  • Interferon chemical made and released by cells
    infected by viruses.
  • When the interferon is released it binds to
    receptors on the outside of neighboring cells.
  • It actually works to block the virus from being
    able to bind to neighboring cells. That means
    that the virus cant infect neighboring cells
    because the attachment sites are taken by
    interferon.
  • It also signals the cell to make antiviral
    proteins that inhibit viral replication.
  • It sounds like a great treatment for viral
    infections but generally it isnt very effective.
    It is thought that the reason is because the
    amount of interferon needed to actually coat the
    cells and keep them continually protected is too
    great to maintain.
  • See Fig. 14.20
  • No HW.
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