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Host Defense > Path V > Flashcards

Path V Flashcards

1
Q

What are the 5 functions of inflammation?

A
  1. dilute (toxins and mediators of inflammation)
  2. destroy- invading organisms
  3. dispose- remove dead tissue, leukocytes, bacteria
  4. develop/prepare tissue for healing
  5. deter: activate, modify, and participate in the establishment of acquired immunity (I guess deter refers to detering future pathogens?)
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2
Q

5 general categories of things that participate in the inflammatory response

A
  1. vascular endothelial cells
  2. vascular basement membrane
  3. ECM
  4. leukocytes
  5. tissue cells
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3
Q

What are the four functions of the chemical mediators of the inflammation?

A
  1. initiate the inflammatory response
  2. amplify it
  3. modify it.
  4. terminate it
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4
Q

What is the first step of inflammation?

A

vascular dilation leading to increased local bloodflow

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5
Q

What 7 factors promote vascular dilation?

A

histamine, NO, bradykinin, PAF, neuropeptides, prostaglandins, lipoxins

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6
Q

What is vascular endothelial activation/damage (3 forms)

A

direct damage, endothelial contraction or cytoskeletal reorganization, or leukocyte directed injury mediated by the release of toxic oxygen species and lysozpmes

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7
Q

What factors medaite endothelial contraction or cytoskeletal reorganization in the vascular endothelial activation?

A

histamine, serotonin, leukotrienes, fibrin split products, PAF

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8
Q

What are the three types of activation in the the vascular endothelial response?

A

redistribution of adhesion molecules on the cell surface, conformational changes leading to increaded binding affinity, and induction of increased numbers of adhesin molecules

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9
Q

What factors promote the vascular endothelial activation?

A

TNF=alpha, IL1, PAF, IL8, IL16, free radicals, leukotrienes, thrombin, factor X

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10
Q

What is P-selectin? What does it do, where is it found?

A

a protein constitutively expressed on endolthelial cells in low amts
stored within weibel-palade bodies within endothelial cells but can be redistributed on to the cell surface.
participates in the rolling phase by binding to leukocyte surface glycoproteins showing sialyl-Lewis X

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11
Q

What factors induce the redistribution of P-selectin to endothelial cell surfaces? (5)

A

thrombin, PAF, INF-gamma, TNF-alphal and IL-1

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12
Q

What is E-selectin? Who does it bind and what does it do?

A

binds leukocyte sialyl-Lewis X even better than P selectin. participates in the rolling and adhesion phase

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13
Q

What factors promote the expression of E-selectin?

A

TNF-alpha, IFN-gamma, IL-1, PAF (JUST LIKE P-selectin)

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14
Q

What is L selectin?

A

present on the sufrace of leukocytes, L-selectin participates in the rolling phase by binding to the groteoglycan GlyCam-1 on endothelial cells

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15
Q

What facorts induce the expression of L-selectin?

A

TNF-alpha, IL-1, PAF, INF-gamma

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16
Q

What is ICAM-1?

A

It is a mediator of firm adhesion. It attaches to integrins MAC-1 on neutrophils and LFA-1 on macrophages and lymphocytes. They are converted to an active for by TNF-alpha, IL-1, and IL8

17
Q

What factors induce ICAM-1 expression?

A

TNF-alpha, IL-8, and IL1

18
Q

What is PECAM-1

A

an adhesion molecule expressed at endothelial cell junctions under influence of TNF-alpha and IL1. It acts as an anchoring system to promote leukocyte transmigration through the endothelial junctions. Binds VLA-4.

19
Q

What are the effects of fluid and protein leakage into the tissues?

A
  1. dilutes the conc. of toxins and CMOIs
  2. allows proteins important to the inflammatory response to get to the site
  3. expands the ECM to allow easier migration of the cellular components of the immune system
  4. larger proteins remain in the vascular space.
  5. relatively greater loss of water leads to incr. intravascular protein/RBC concentrations so even with incr. blood vol reaching the area the blood flow becomes more sluggish (more sluggish blood flow)
20
Q

What is margination of leukocytes?

A

leukocytes travel along the vessel walls instead of in the central flow

21
Q

What 5 favors lead to leukocyte margination?

A

increased total blood flow

  1. intravascular fluid loss
  2. slower flow
  3. incr. in cell and plasma protein conc.
  4. pronounced axial flow of RBCs.
22
Q

What is leukocyte rolling? What interaction mediates this event?

A

activated endothelial cells interact with marginated leukocytes
this slows down the leukocytes
medated through P-selectin on endothelial cells and sialyl-Lewis X on leukocytes

23
Q

When does leukocyte activation occur? How?

A

occurs during or before rolling phase
prepares for firm adhesion to the endothelium by increasing sialyl-Lewis X on glycoproteins and L selectins and integrins conformational change

24
Q

What is the purpose of leukocyte activation?

A

primes the locomotion nad bacteriocidal mechanisms of the cells and increases the energy production and O2 consumption by the leukocytes

25
Q

What is leukocyte adhesion? Between molecules do we see this?

A

firm attachement of the clel to the endothelium to allow for initiation of the transmigration process
Between endothilail ICAM 1 and MAC for neutrophils
between ICAM1 and LFA 1 for macros and lymps
between E-selectin and sialyl Lewis X interactions

26
Q

Where does transmigration take place?

A

in the post-capillary venules

27
Q

What helps with lekuocyte transmigration? (4)

A

gaps widened between the endothelial cells, locomotion of activated leukocytes, expression of adhesion molecs at the endothelial cell junctions like PECAM-1 and proteolytic enzymes made by leukocytes to separate cells and breakdown the basement membrane

28
Q

What is the definition of leukocyte migration?

A

locomotion of leukocytes through the extravascular matrix following a chemotactic gradient

29
Q

What interactions are important for leukocyte migration?

A

cell integrins with ECM components like fibronectin, integrins, and hyaluronan

30
Q

What initiates leukocyte movement and chemotaxis?

A

activation of phospholipase C via a G-proptein dependant receptor. leads to an influx of extracellular Ca and the release of internal Ca stores. this Ca allows for the assembly and activation of actin-myosin contractile elements that help leukocytes move via pseudopodia formation.

31
Q

What is the first step of leukocyte phagocytosis and killing?

A

activation, recognition, and attachment.

32
Q

How might a leukocyte recognize bacterial or other pathogenic bad guys?

A

Toll like receptors, G-protein coupled receptors, MAC-1 integrins (non-specific). Or, opsonins. Opsonins bind microorganisms and help them bind to specific receptors on the leukocytes.

33
Q

What are three major opsonins?

A
  1. collectins
  2. antibodies
  3. complement fragments C3b and C3bi.
34
Q

What are collectins?

A

proteins which bind to exclusive bacterial carbohydrates like mannos, then bind complement, and bind C1 receptors.

35
Q

What two factors trigger phagocytic engulfment?

A

binding, as with Fc receptors

binding opsonins with additional stim by binding other factors (Extracellular fibronectin, lamellin, or cytokines).

36
Q

What mediates engulfment?

A

increased cytosolic Ca associated with G-protein/phopholipase C activation

37
Q

How do phagocytes KILL things>

A

increased glycolysis and O2 consumption –> “oxidative burst”
this generates H2O2, via NADPH oxidase

38
Q

Through what three mechanisms is H2O2 killing of bacteria enhanced?

A

Fe++ oxidation to make OH radical from H2O2
Haber-Weiss rxn (also makes OH radical)
myeloperoxidase from azurophilic granules makes HOCl, aka clorox bleach

Host Defense (38 decks)

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