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59 Cards in this Set

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Physiological basis for response
Triggered by injury or infection
Restrict tissue damage to site of infection or injury and stimulates tissue repair
Acute inflammation sequential order
neutrophils
Macrophages
T cells
Chronic inflammation
persistent antigen can't be cleared
What are the cells that release mediators
1. Mast cells
2. Neutrophils
3. Macrophages
4. Eosinophils
5. T cells
6. Platelets- strictly speaking- lack nuclei
CHEMOKINES are subset of cytokines
induce chemotaxis
Extravasation of toxins

Cells migrate along these chemokine gradients

They are important for triggering change of infinities low to high affinity triggered by EC chemokines binding to leukocytes.
What are the major groups of chemokines
1) C-C Chemokines
2) C-X-C chemokines

according to cytosine positioning
C-C chemokines examples:
MIP1 alpha
MIP1 beta
Rantes
Eotaxin

aka CCLX
CCLx
C-C chemokines
C-C chemokines

MEN- MTB
secreted by macrophages, neutrophils and endothelial cells

Chemotactic for
1) macrophages
2) T and B cells
XXC Chemokines
iL8 trigger change of infinity in integrins

ITAC (CXCl1)
IP-10 (CXC10)
What secretes CXC cehmokines
Fibroblasts
Endothelial Cells
macrophages
What are CXC's chemotactic for?
Neutrophils
Basophils
T cells (10 and 11)
What are CC chemokines chemotactic for?
Macrophages
T and B cells
What releases CC chemokines?
Macrophages
Endothelial Cells
Neutrophils
KININ SYSTEM
Enzymatic cascade in plasma
Generates bradylkinin which causes

permeability, dilation, pain

REDNESS, PAIN, SWELLING
KININ SYSTEM Symptoms
Redness, Pain, Heat and Swelling
Enzymatic cascade in the plasma is also known as
CLOTTING system
FIBRINOGEN
converted to fibrin for converting system via THROMBIN
FIBRIN
makes clot and prevents blood loss
Fibrin is chemotactic for
NEUTROPHILS (1st response)
Clotting system is also pro...
Angiogenic

Angiogenesis: generation of new blood vessels

Fibrin good at simulating new blood vessel growth, for healing of wound
Complement system as mediator
Generates anaphylatoxins (c3a, 4a,5a)
Mast cells de-granulate = bursting of all vesicles release HISTAMINE
Mast cells degranulation release
HISTAMINE
Anaphylatoxins (3a,4a,5a) are chemotactic for
NEUTROPHILS
What cleaves lipids?
Macrohages
Neutrophils
What is cleaved into protaglandins and leukotrienes
Arachidonic acid is cleaved into pge2 and ltb4
Pge2 and ltb4 downstream effects
dilation, permeability, neutrophils,
pge2 and ltb4 indirect responses?
PAIN
What enzyme is upstream of pge2?
COX 1 and Cox2
what drug is associated with Cox 1 and Cox 2?
ADVIL
Players for lipid mediators
arachidonic acid
COX 1/2
pge2 and ltb4
prostalaglandins and leukotrienes
Xox 1 web definition
An agent that inhibits the action of the enzyme cox-1 (cyclooxygenase-1). The common anti-inflammatory drugs such as aspirin, ibuprofen, and naproxen block the action of both cox-1 and cox-2. Cox-1 inhibitors can reduce inflammation, but they may also decrease the natural protective mucus lining of the stomach. Therefore, these medications can cause stomach upset, intestinal bleeding, and ulcers. In some cases, using a buffered form of a cox-1 inhibitor can eliminate or reduce these adverse effects.
Cytokines are last mediator of inflammation
1, 6
TNF, IFN gamma
Neutrophils
First cells that go to infected/damage site
When does neutrophil influx peak
6 hours, then thought to decline after
Affinity of neutrophils
10 to the 11th power
How are neutrophils recruited?
E and P selectin
as they express ligand for these
What is the particular ligand Neutrophil uses to get recruited to tissue?
PSGL-1
Extravasation is the same except
after entering tissue follow 83 highway
il8-3 gradient (higher concentration)
Following 83 gradient will lead the neutrophils to
RESPIRATORY BURST where they generate ROI: reactive oxygen intermediates
ROI
Reactive oxygen intermediates

Kill anything and everything around us
What is the result of ROI?
PUS after neutrophils explode
Specificity of neutrophils?
they aren't androgen specific, so they kill whatever is around.
Accute response long mechanism
antibodies bind to bacteria
tissue damage initiates C'(3a, 5a)
c' and mast cells

Mast cells release histamine and pge2
accite response long mechanism 2
endothelial cell E-selectin and neutrophil ligand (psgl1) drive migrationi nto tissue
Acute inflammation and macrophages
mphages will be phagocytosing bacteria and generating lipid mediators pge2
Acute inflammation and pge2
Affects endothelial cells
Macrophages make 1, TNF, 6
Acute inflmmation and cytokines
upregulated 1 TnF and 6 which regulate EC and cause neutrophil, T cells and macrophages to migrate into tissues
What kind of gradient darw cells in
ANAPHYLATOXINS from C' and chemokines (macrophages)

T cells- IFN gamma
Tissue or Ec damage causes
fibronogen to fibrin via thrombin (clotting)
EC damage leads to
Bradylkinin (kinin system)
permeability, dilation pain
WHAT IS A GOOD NEGATIVE REGULATOR OF IMMUNE RESPONSE?
TGF-beta
Stimulates tissue repair
Good to repai after you get rid of bacterial infection
Chronic inflammation
DTH
Unmovable antigen/stimulant

response of a lot of activated macrophages
Chronic inflammation constantly activates
macrophages and T cells
Macrophage build up during Chronic inflammation
GRANUOLA- Tuberculosis
Chronic inflammation cells and cytokines
macrophages and T cells
TNF and IFN gamma
Aspirin
irreversibly inhibits COX1
Blocks ability to generate lipid mediators
NSAID examples
ibuprofin, alieve, nanproxyn
NSAIDS are good at
reducing inflammation pain

swelling
leakage
blood flow

Reversibly inihibits COX1 (enzyme for conversion)