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chapter 16
Fichas del conjunto (40)
- 1innate immunitydefense against any pathogen, nonspecific without memory. physical barriers (external), chemical mediators (internal, external), cells involved in phagocytosis and production of chemicals for the immune response (internal)
- 2marginationblood flow decreases as phagocytes stick to the inner lining of blood vessels
- 3PAMPsPathogen-associated molecular patterns
Structurally conserved molecules derived from microbes - 4TLR'ssingle, membrane-spanning, non-catalytic receptors that recognize structurally conserved molecules (PAMPs) derived from microbes, which activate immune cell responses, resulting in secretion of cytokines
- 5identify physical examples of the 1st line of defenseskin epidermis consists of keratin, a protective protein
mucous membranes--mucous traps microbes
ciliary escalator---lacrimal apparatus--washes eye
saliva, washes microbes off
urine/vaginal secretions---flow out
peristalsis--defecation, vomiting - 6identify chemical examples of the 1st line of defensefungistatic fatty acid in sebum
low ph (3-5) of skin
lysozyme in perspiration, tears, saliva, and urine
low ph (1.2-3.0) of gastric juice
low ph (3-5) of vaginal secretions - 7identify the effects of the following chemical mediator: complement proteinsopsonization or immune adherence: enhanced phagocytosis
membrane attack complex: cytolysis attract phagocytes - 8identify the effects of the chemical mediator: cytokienesproteins that regulate the intensity and duration of immune response, isolate and destroy microbes
- 9identify the effects of the chemical mediator: histaminechemical released by activated mast cells that increase the flow of blood and fluids to the surrounding area
- 10identify the effects of the following chemical mediator: interferonsinterfere with viral replication with cells
- 11identify the effects of the following chemical mediator: kinininduce vasodilation
- 12identify the effects of the following chemical mediator: luekotrieneshaving a chemotactic effect on migrating neutrophils, as such help to bring the necessary cells to the tissue as do kinins.
in addition, leukotrienes also help attach phagocytes to pathogens - 13identify the effects of the following chemical mediator: lysozomeenzyme, present in mucous, tears, and saliva, that destroys bacteria by dissolving their cell walls (lyse cells)
- 14identify the effect of the following chemical mediator: prostaglandininflammation-related: : from damaged cells,
intensifies histamine action and attracts
phagocytes - 15identify ways in which normal microbiota provide protection from infectioncompete with pathogens or alter the environment
lactobacillus acidophilus prevents growth of Candida albicans by creating a more acidic environment, which does not allow it to thrive, preventing a yeast infection
e.. coli produce bacteriocins which inhibit salmonella and shigella growth - 16neutrophils1st to respond, stay in circulation 10-12 hours, survive 1-2 days after leaving circulation
secrete lysozome
become motile, phagocytize bacteria, antigen-antibody complexes and other foreign matter - 17eosinophilsleave circulation and enter tissues during inflammatory response
prevalent in allergic (hypersensitivity) reactions
destroy inflammatory chemicals like histamine via enzymes
release chemicals that help destroy tapeworms, flukes, pinworms, and hookworms - 18basophilsleast common
leave circulation and migrate through tissues
play a role in both inflammatory response and allergic reactions
produce histamine and heparin - 19lymphocytessmallest WBC's
produced in red bone marrow but then migrate to lymphatic tissues and proliferate
responsible for antibody production
studied extensively with the immune system - 20monocyteslargest WBC's
remain in circulation for 3 days, leave circulation and become macrophages
increase in numbers associated with chronic infection
phagocytic cells
can break down antigens and present them to lymphocytes for recognition - 21identify the WBC responsible for phagocytic activity in early stage vs late stages of infectionneutrophils are responsible for phagocytic activity during the early stages of infection and monocytes are responsible for phagocytic activity during late stages
- 22identify the steps involved in phagocytosis1. chemotaxis and adherence of microbe to phagocyte
2. ingestion of microbe by phagocyte
3. formation of a phagosome
4. fusion of the phagosome with a lysosome to form a phagolysosome
5. digestion of ingested microbe by enzyme
6. formation of residual body containing indigestible material
7. discharge of waste materials - 23identify means by which pathogens prevent any step(1) inhibit adherence: M protein, capsules
(2) Kill phagocytes: leukocidins
(3) lyse phagocytes: membrane attack complex
(3a) escape phagosome and prevent phagosome-lysosome fusion
(4) survive in phagolysosome--like the low pH - 24how can bacterial enzymes such as catalase and superoxide dismutase protect bacteria from phagocytic digestion?these products are then used by other cell enzymes to destroy ingested microbes. bacteria equipped with enzymes such as catalase and superoxide dismutase are able to neutralize these toxic forms of oxygen
- 25present in high abundance during allergic reactionsbasophils and eosinophils
- 26present in high abundance during parasitic worm infectionseosinophils
- 27from which macrophages arisemonocytes
- 28from which dendritic cells are derived frommonocytes
- 29identify functions of inflammation(1) acute-phase proteins activated>>
complement, cytokine, and kinins
Vasodilation: histamine, kinins, prostaglandins, and luekotrienes
Characterized by 4 signs/symptoms: redness, swelling (edema), pain, heat
occasionally: loss of function - 30how does a fever arise?the body's thermostat (hypothalamus) is reset upwards in response to cytokines (pyrogens), chemicals secreted by leukocytes and macrophages exposed to bacteria and other foreign substances.
As a result of resetting the body's thermostat, the body responds with vasoconstriction, increasing the body's metabolic rate, producing a chill (fever) - 31why does a chill indicate that a fever is about to occur?As a result of resetting the body's thermostat, the body responds with vasoconstriction, increasing the body's metabolic rate, and shivering (metabolic activity), all of which produce additional heat. And yet, the skin remains cold, is a clear indiction that body temperature is rising and will continue to do so until body temperature reaches a new thermostat level at which the chill disappears. The thermostat remains at this higher temperature until cytokines are eliminated. To get rid of this excess heat, blood vessels dilate and sweat production increases. This phase of the fever in which body temperature is falling is called "crisis."
- 32What does it mean when it says that the complement system acts in a cascade?complement proteins are activated in a sequence (meaning that the activation of one cannot occur until the one before is activated and once it has, it triggers the activation of the subsequent complement protein)
- 33identify the three ways in which the complement proteins destroy mcirobesinflammation
opsonization
form membrane attack complexes (MAC) - 34activation of C3a and C5a triggers what?bind to mast cell receptors which cause mast cells to release histamine and other chemicals that increase blood vessel permeability during inflammation
additionally, c5a acts as a strong chemotaxin for phagocytic cells - 35activation of c5-c9 triggers whattriggers the formation of the MACs which forms a channel through the membrane
- 36activation of C3b triggers what?along with activating c5 protein to split into c5a and c5b, c3b also coating microbes' surfaces, making them easier for macrophages to engulf (opsonization)
- 37activation of C5a triggers what?bind to mast cell receptors which causes mast cells to release histamine and other chemicals that increase blood vessel permeability during inflammation. additionally, C5a acts as a strong chemotaxin for phagocytic cells
- 38*how does opsonization help enhance phagocytosis?*fragments bind to the microbial surface to which a phagocytic receptor can adhere to
- 39at which point in the 3 complement activating pathways cascade all 3 activating mechanisms the same?after the activation of c3, all pathways are the same
c3 splits into c3a and c3b, c3b activates c5 protein to split into c5a and c5b, c3b also coating microbes' surfaces, making them easier for macrophages to engulf (opsonization)
c3a and c5a bind to mast cell receptors which causes mast cells to release histamine and other chemicals that increase blood vessel permeability during inflammation. additionally, c5a acts as a strong chemotaxin for phagocytic cells
c5b activates c6, c7, c8, and c9 forming MACs - 40in detail: how do the three compliment pathways differ?Classical Pathway--the variable region of the antibodies binds to the epitope of the pathogen. C1 binds to the constant region which activates C2 and C4 to split into C2a, C2b, C4a, and C4b. C2a and C4b activate C3.
Lecting pathway--Lectin binds to mannos on the invading cell. Lectin activates C2 and C4 to split into C2a, C2b, C4a, and C4b. C2a and C4b activate C3.
Alternative Pathway: Factors B, C, and P on the surface of the membrane activate C3.
Información
- Descripción
- Fichas sobre chapter 16, creado por newsha el 07/11/2014.
- Creado por
- newsha · nov 2014
- Actualizado
- 19 feb 2016
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