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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.

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Presentation on theme: "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."— Presentation transcript:

1 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. 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 can’t 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): 2 nd 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 body’s 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 doesn’t 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 body’s 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 can’t 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 isn’t 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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