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immunology 4 Flashcards

inflammation (local v systemic) chronic and acute

1
Q

what is the stereotypical pathway of acute inflammation?

A
  1. Local tissue damage
  2. vasodilation
  3. erythma (rubor)–redness
  4. increase in temperature (calor)
  5. increase in capillary permeability, fluid accumulation (swelling pain)
  6. Continued chemotaxis
    * accumulation of immune cells could lead to increase inflammation
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2
Q

what is local inflammation?

A

it happens in one area and is characterized by an increase in vascular permeability and vasodilation and that equations to an increase of immune cells into the tissue and a decrease in blood pressure. it also recruits immune cells. it also releases cytokines and effector molecules and could potentially lead to thrombosis.

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3
Q

what is systemic inflammation?

A

not just one site and is characterized by fever

proliferation of immune cells and synthesis and release of immune mediators from distal organs not adjacent organs.

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4
Q

what is exudate?

A

extravascular fluid with proteins and cells.

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5
Q

what is an edema?

A

excessive fluid in interstitial tissue

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6
Q

what are inflammatory cytokines?

A

IL-6, TNF-alpha, IL-1beta, CXCL8, IL-12

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7
Q

how are inflammatory cytokines involved?

A

they help mobilize neutrophils, activate vascular endothelium, and chemotactic.

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8
Q

what does IL-6 do and is it involved in local and systemic inflammation?
what secretes them?

A

IL-6 is used in local inflammation.
It induces fever and starts APP production by hepatocytes.
macrophage

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9
Q

what does IL-12 do and is it involved in local and systemic inflammation?
what secretes them?

A

IL-12 is used in local inflammation.
It is used to activate NK cells
macrophage

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10
Q

What does TNF-alpha do and is it involved in local and systemic inflammation?
what secretes them?

A

it is used in both local and systemic.
LOCAL: Turn on vascular endothelium, increase vascular permeability which increases the entry of complement and cells to tissue and it increases the fluid sent to the draining lymph node.
SYSTEMIC: Shock, fever, and mobilization of metabolite
Macrophage.

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11
Q

what does IL-1beta do and is it involved in local and systemic inflammation?
what secretes them?

A

It is used in both.
LOCAL: Activate vascular endothelium, active T and B cells, local tissue destruction, increase access to effector cells because of vascular endothelium.
SYSTEMIC: Fever, production of IL-6
Macrophage.

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12
Q

what does CXCL8 do and is it involved in local and systemic?

what secretes them?

A

It is used in local effects. It is a chemotactic factor that helps recruit neutrophils and basophils to the site of infection.
macrophage.

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13
Q

what is the purpose of endothelium in inflammation?

A

it lines blood vessels.
expresses adhesion molecules for leukocytes (increase by TNF-alpha and IL-1)—slow down and contact endothelium walls to get access to them.
produce pro-inflammatory cytokines–increase chemotaxis, start angiogenesis for tissue repair

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14
Q

what is the purpose of platelets in inflammation?

A 
help blood clot
They release:
ROS-to get more platelets
FIBROBLAST GROWTH FACTOR-wound repair
SEROTONIN:help vasodilation
ANTI-MICROBIAL PEPTIDES
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15
Q

what is the purpose of neutrophils in inflammation?

A

attracted to tissue because of CXCL8
active phagocyte in tissue
kill by ROSS and granules
release IL-8

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16
Q

what is the purpose of macrophages in inflammation?

A

ingest microbes and damaged cells
produce IL-6, TNF-alpha, and IL-1
produce growth factors that help in repair

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17
Q

what is the purpose of eosinophils in inflammation?

A

eosinophils release cytokines, leukotrienes, and prostaglandins.

18
Q

what is the purpose of basophils in inflammation?

A

relese histamine and heparin.

19
Q

what is the purpose of mast cells in inflammation?

A

release histamine, TNF-alpha in an allergic response or pathogen invasion.

20
Q

describe leukocyte migration.

*local

A
  1. leukocyte will attach to the wall ad integrins and glycoproteins will be released.
  2. leukocyte will roll down
  3. integrin on outside will turn on and bind–inside out signal change.
  4. Leukocyte will eventually get really ‘sticky’ and will stop and flatten.
  5. Leukocyte will be integrated through PCAM that secreted enzymes that break the wall and into the tissue to let chemokines flow to the site of infection.
  6. chemotaxis follow
  7. macrophage eat and upregulat p selectin and release TNF, IL-12 to widen blood vessels and decrese blood flow—let things bind since flow isn’t as fast.
21
Q

what is the purpose of macrophage and neutrophil activation?

*local

A

They release cytokines and chemokines and they bind to PAMPs and DAMPs that activate leukocytes.
they increase endothelial binding and transmigration
increase phagocytic activity
upregulation of phagocyte oxidate/iNOS, ROS, RNI pumped into phagosome.
Netosis of neutrophils
release pro-inflammatory cytokines and release DAMPs.

22
Q

what is histamine and define purpose?

*local

A

histamine is a granule released from the mast cell and offer quick and early mediatory of increase in vascular permeability.

23
Q

how does blood clotting help in inflammation?

*local

A

a blood clot is a physical barrier and it blocks access of infectious agents and helps contain them. some can make the infection part of the log.
if the clot is not made well then bacteria can go around it and spread and that can be dangerous.

24
Q

how does arachidonic acid metabolites control inflammation?

*local

A

Arachidonic acid can make cyclooxygenase which can make prostaglandin G2 and then prostaglandin H2. This in turn can make Prostacyclin PGI2, thromboxane A2 TXA2 and PGD2 and PGE2.
It can also make 5-lipoxygenase that makes 5-HPETE that makes leukotriene A4 and B4. Leukotriene A4 can make leukotriene C4, Leukotriene D4 and leukotriene E4 which all deal with broncheospasm, increased vascular permeability—eventually ASTHMA
it can also be anti-inflammatory through 12-lipoxygenase (lipoxin A4 and Lipoxin b4)

25
Q

what does prostacyclin PGI2 do? *local

A

it causes vasodilation and inhibits platelet aggregation

26
Q

what does thromboxane A2, TXA2 do? *local

A

it causes vasoconstriction and promotes platelet aggregation

27
Q

what does PGD2 and PGE2 do? *local

A

causes vasodilation and increased vascular permeability

28
Q

what do acute phase proteins do and what cytokines stimulate them?

A

Acute phase proteins help with:
clotting (fibrogen)
help with immune cell homing (serum amyloid A)
bind phosphocholine, activate complement (creatine protein)
complement (C3 help make complex)
bind free hemoglobin, sequester Fc (haptoglobin.
CYTOKINES: IL-1, IL-6, TNF

29
Q

is systemic inflammation just an increase in local inflammation over time?

A

yes.

30
Q

what are tests we could do to test for systemic inflammation?

A 
C reactive Protein (CRP)
Erythrocyte sedimentation rate (ESR)
D-dimer
CBC with differential
TEMP.
31
Q

how can C reactive protein help?

A

liver produced opsonin and production increased by IL-6

32
Q

how can erythrocyte sedimentation rate (ESR) help?

A

fibrogen aggregates in RBC and settle suspension

33
Q

how can D-dimer help?

A

degradation of fibrin, indicates clot formation

34
Q

CBC with diff help?

A

could elevate proliferation of immune cell types in response to infection.

35
Q

how does the body stop or control inflammation?

A

Pathogens hopefully eliminated
cytokines/app have short half lives
effectors can also immunosuppress (NOS) help stop proliferation.
neutrophils have short lives and are cleared by macrophages
activated cellular signaling proteins either deactive or degrade (stop TLR pathways)
macrohages release growt factors (TGF-beta) and metabolites, recruit fibroblasts, relese Il-10 (anti inflammatory) and express suppressive cell surface ligands (stop leukocyte roll)
suppressive cells (TREGS) release immuno-modulatory cytokines [IL-10]

36
Q

what is the mediator, initiator and symptoms of arthritis?

A

lymphocytes, macrophages
autoimmunity
joint, inflammation pain

37
Q

what is the mediator, initiator and symptoms of asthma?

A

eosinophils, IgE
allergen, irritant
airway inflammation

38
Q

what is the mediator, initiator and symptoms of atherosclerosis?

A

macrophages
oxidized LDL uptake by macrophages
clogged airways

39
Q

what is the mediator, initiator and symptoms of chronic transplant rejection?

A

lymphocytes, cytokines
lymphocyte response to transplanted tissue
fibrosis of the vessels of the transplanted tissue

40
Q

what is the mediator, initiator and symptoms of pulmonary fibrosis?

A

macrophages, fibroblasts
inhalation of pollutants, cigarette smoke
scarring in the lung.

FMS (5 decks)

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