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Block 1 Week 5 > Inflammation 2 > Flashcards

Inflammation 2 Flashcards

1
Q

what does a successful inflammatory response do? an unsuccessful one?

A
  • a successful inflammatory response to perturbation (injury, infection) restores homeostasis
  • a pathological inflammatory response results in tissue damage and/or tissue remodeling
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2
Q

tissue remodeling

A
  • development of new specialized cell types

- scarring or alteration of tissue function due to poor inflammatory response

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3
Q

tissue homeostasis

A
  • regulation of normal tissue state

- tissue undergoes cell death & repair w/o causing problems when old or damaged

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4
Q

what is acute inflammatory response thought to be associated with?

A
  • bacterial infections

- can also be due to stress or trauma; but typically if see acute response, assume bacterial

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5
Q

feed forward mean?

A
  • is the idea that we can activate responses and products of the response (IL-1b or TNFa inflamm cytokines) can induce other cells to make more of it
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6
Q

feedback mean?

A
  • production of a molecule leads to feedback inhibition of the initial trigger
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7
Q

feedback and feed forward processes?

A
  • can have both going on at same time in certain pathways

- can be targets for therapeutic interventions in inflammation

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8
Q

5 clinical signs of acute inflammation?

A

1) Rubor (redness)
2) Calor (heat)
3) Tumor (swelling)
4) Dolor (pain)
5) laese functio (loss of function)

  • most due to blood vessel responses*
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9
Q

Rubor

A
  • redness in the skin
  • increased blood flow= increased color
  • smooth muscle in arterioles is relaxing causing increased diameter so blood can rush to area of inflammation
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10
Q

calor

A
  • heat
  • increased local blood flow= increased local temperature
  • due to dilation, blood form our core (warmer blood) is moving to areas of inflammation faster so feel warmth
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11
Q

Arteriole vs venule? clinical features of inflammation involving which one?

A
  • arteriole is higher pressure vessel ( involved in transudate)
  • venule is thinner walled & no smooth muscle layer (involved in exudate)

clinical features in inflammation are due to arteriole changes

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12
Q

tumor

A
  • swelling (edema)
  • increased blood flow, causes changes in vascular permeability
  • fluid can leak from blood vessels into extracellular matrix -causes the loose connective tissue to expand= edema
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13
Q

Two ways vascular circulation can contribute to extracellular fluid?

A

1) transudate

2) exudate

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14
Q

transudates

A
  • swelling/edema
  • due to altered balance between hydrostatic & osmotic pressure that pushes water and ions out of arteriole and into loose connective tissue
  • (increased hydrostatic or decreased osmotic)
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15
Q

lymphatics & transudates

A

-lymphatics help remove some of the excess fluid transudates push into the connective tissue to release swelling during an inflammatory response

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16
Q

exudate

A
  • swelling/edema
  • due to induced changes in vessel permeability
  • loose barrier function of endothelium (due to inflam toxic factors etc.)
  • lead to direct leakage of H20 and serum, proteins, cells etc,
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17
Q

Exudation due to increased vascular permeability is due to what?

A
  • can be from different inflammatory-induced effects
    1) chemical mediators
    2) chemical, toxin, or physical damage
    3) leukocyte-mediated
    4) endothelial transcytosis (loose epithelial barrier)
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18
Q

chemical mediators of exudation?

A
  • Histamine
  • common source= Mast cells
  • can bind receptors at sites of inflammation & cause smooth muscle relation & vessel dilation
  • results in swelling (tumor), and rash sometimes
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19
Q

steps for histamine release?

A
  • mast cell is common source
  • if have allergic response, IgE binds receptors, causes degranulation of mast cells, histamine released
  • results in swelling (tumor), and rash sometimes
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20
Q

dolor

A
  • pain

- can be caused by number of things including Arachidonic Acid (AA) metabolites

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21
Q

recruited leukocytes functions

A

1) production of cytokines to drive tissue responses
2) filling infectious microbes,
3) removal of cell debris

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22
Q

blood flow and inflammation

A
  • classic sign of inflammation= recuritment of cells from blood
  • heart pumps lymphocytes & neutrophils through blood, allows first responders to get to inflammation site ASAP
  • poor profusin can impair inflamm response
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23
Q

neutrophils

A
  • first responder
  • rapidly recruited
  • short lived (12-18hr)
  • can enter, handle infection, eat up bacteria but arent actually clean up crew for the left over dead bacteria
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24
Q

macrophages

A
  • later part of inflamm response -clean up crew of old dead bacteria left behind by neutrophils
  • longer lived, can differentiate into specialized roles in clean up, wound repair & remodeling
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25
Q

What is pus?

A

-when have an accumulation of phagocytic cells that are killing bacteria, then leaving it and not enough macrophages to clean up bacterial remains

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26
Q

what inflammatory cells are recruited from the blood?

A

1) Red cells (erythrocytes)
2) Platelets
3) White cells (leukocytes)
Neutrophils* (polymorphonuclear leukocytes, polys, pmn, granulocytes)
Eosinophils
Basophils
Monocytes*
Lymphocytes

27
Q

What are the 5 types leukocytes (white cells)

A 
1) Neutrophils
(polymorphonuclear leukocytes, polys, pmn, granulocytes)
2) Eosinophils
3) Basophils
4) Monocytes
5) Lymphocytes
28
Q

which leukocytes are phagocytic?

A

1) neutrophils
2) monocytes
* both are first responders

29
Q

polymorphonuclear leukocytes

A
  • have segmented nucleus,
  • when bone marrow pumping out immature neutrophils in infection, nucleus doesn’t have time to segment, so looks like a horseshoe called bands
30
Q

how leukocyte know where to stop and exit from blood stream which is moving very quickly?

A
  • endothelium has molecules that can display in luminal side of vessel to trap circulating cells & cause them to slow (rolling) & get across blood vessel
  • have chemoattractant signals on blood vessel walls, provide direcitonal role to direct cells where to go
31
Q

mechanism of getting leukocyte to site of inflammation, and from blood–> tissue?

A

1) selectins P & E bind to glycoprotein counterreceptors on leukocytes, slows them down, additional molecules can then bind
2) binding events can trigger leukocyte to express more receptors (for adhesion molecules)
3) Chemokines(produced in inflamm tissue) picked up by vascualr endothelium & displayed
4) leukocyte can migrate (roll) down endothelial w adhesion molecules, find where need to, leave blood & enter tissue

32
Q

Chemokines & leukocyte recruitment?

A
  • chemokines produced in inflamm tissue picked up by vascualr endothelium
  • transported across cell & displayed on luminal side
  • are chemoattarctant signals for cells, tells them to adhere & roll and provides directions to cells (roll toward the chemokines)
33
Q

Selectins and 3 types?

A
  • leukocyte and endothelial proteins that mediate cell adhesion to carbohydrates
    1) P-selectin
    2) L-selectin
    3) E-selectin
34
Q

P-selectin? how long dominant after stimulus?

A
  • on endothelia and platelets, upon activation rapidly transferred to cell membrane
  • dominant up to 1 hour after stimulus
35
Q

L-selectin

A

-on leukocytes, expressed constitutively, become more adhesive in stimulated leukocytes but shed within minutes of activation

36
Q

E-selectin? how long dominant after stimulus?

A
  • on endothelia, induced within hours by inflammatory mediators
  • dominant at later time points
37
Q

Selectin Function

A

1) Bind specifically to sugars in glycoprotein counter receptors on leukocyte
2) mediate the initial contact of leukocytes with endothelium in the area of inflammation (rolling)
3) help leukocytes slow down

38
Q

Integrins

A
  • family of receptors involved in surface & target recognition & adhesion by inflammatory cells
  • ON INFLAMM CELLS*
  • Heterodimeric (alpha&beta subunits)
  • involved in inflammation, embryogenesis, tumor invasion, hemostasis, wound healing
  • can also provide signals to cells
39
Q

Integrins heterodimer structure and what do they bind to?

A

structure: alpha and beta subunits (11 alpha, 7 beta)
bind to:
1) extracellular matrix proteins
2) microbial structures
3) specific counterreceptors on endothelial & other cells

40
Q

Integrin Function

A

1) help inflammatory cell adhere to ligands
2) signals to the cell when ligands engage the receptor
3) signaling from the cell to the receptor to regulate its adhesiveness for ligands

41
Q

Chemotaxis

A
  • movement of cell in a direction corresponding to a gradient of increasing/decreasing concentration of a a chemokine
  • involved in segregation of lymphocytes into lymphoid tissue
  • chemoattractants signal for leukocytes to come to them
42
Q

what is recruitment of leukocytes directed toward?

A
  • a gradient of chemoattractants
43
Q

chemoattractants include?

A

1) molecules produced by microbes
2) activated complement components
3) lipid mediators
4) small chemotactic peptides called chemokines

44
Q

what type of receptors do chemoattractants have?

A

-G-protein-coupled receptors, which are seven-transmembrane proteins that trigger several signaling events

45
Q

What signaling events do GPCRs activate?

A

1) regulation of actin polymerization& cell motility
2) induction of changes in adhesion molecule activity
3) induce neutrophil activation & degranulation

46
Q

what are the 3 neutrophil effector mechanisms?

A

1) Phagocytosis
2) Secretory Granules
3) Neutrophil Extracellular Traps (NETs)

47
Q

neutrophil Phagocytosis effector mechanism?

A

-can eat up bacteria, but then require macrophages to clean up the dead bacterial remains or get pus

48
Q

neutrophil secretory granules effector mechanism?

A

-granules contain anti-microbial functions & enzymes that actiavte ROS production

49
Q

NETs

A

Neutrophil Extracellular Traps
-Upon specific triggers; neutrophil explodes, nucleic acids from nucleus & histones are released from cytoplasm, form network, trap bacteria & hold them then kill them

50
Q

what is acute inflammation typically caused by?

A
  • bacterial infection or tissue damage & runs a short time course (hence “acute”)
51
Q

acute inflammation in histology vs chronic?

A
  • acute inflammatory infiltrates are dominated by neutrophils
  • chronic inflammation infiltrates are dominated by lymphocytes and mononuclear cells
52
Q

what happens if acute inflammation that fails to resolve infection?

A

-progression to chronic inflammation and/or fibrosis

53
Q

6 ways to reverse acute inflammation?

A

1) clearance of bacteria/cell debris
2) desensitization of receptors for pro-inflamm responses & inflamm cell recruitment
3) Regulation of trxn factors (NF-kB) driving inflammation-associated gene expression
4) Expression of proteins to suppress signaling & inflamm factors
5) Activation of cells to suppress inflammation
6) Programmed Resolution

54
Q

neutrophils &reversal of acute inflammation?

A
  • neutrophils are short lived; can rely on possibility that neutrophils will die and not perpetuate tissue damage cycle
  • unless source/trigger of inflam persists then bone marrow will keep producing new neutrophils
55
Q

Lipid Mediators of Programmed Resolution

A

-conversion of neutrophils to alternative synthesis pathways
(lipoxins, resolvins & Maresin) w/ diff lipid precursors
-have direct effect on inflammatory and scavenger cells
-can suppress neutrophil chemotaxis & activate macrophage reoslution

56
Q

Reversal of NF-kB Activation by IkB

A
  • NFkB activation triggers pro inflam cytokines
  • IkB inhibits NFkB by binding to heterotrimers p65/p50
  • when NFkB activated & enters nucleus, also unregulated IkB production
  • IkB when hit certain level can then enter nucleus, bind NFkB and stop it’s trxn of pro-inflame cytokines
57
Q

Autophagy? what gene is critical for its function?

A
  • cellular process to deliver cell components to autolysosomes for degradation
  • gene ATG16L1
58
Q

3 roles of autophagy

A

1) Clearance of long lived proteins &aggregates

2) role in anti-microbial response: degradation

59
Q

Crohn’s disease and autophagy?

A

-ATG16L1 gene mutants are at increased risk for Crohn’s Disease

60
Q

Lipid Mediators of Programmed Resolution affect on macrophages? neutrophils?

A

1) suppress neutrophil chemotaxis (recruitment of neutrophils)
2) increase macrophage scavenger activity

61
Q

Actions of Lipoxins and Resolvins

A

-direct action to suppress neutrophil recruitment, increase macrophage scavenger activity

62
Q

macrophages help with resolution?

A
  • can target for scavenger activity/degradtion

- clean up apoptotic neutrophils, which helps remove proinflamm stimuli as well

63
Q

what is acute inflammation distinguished by?

A

-rapid onset and rapid resolution

Block 1 Week 5 (8 decks)

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