Immunology And Inflammation

Front 1

Physiological basis for response

Back 1

Triggered by injury or infection
Restrict tissue damage to site of infection or injury and stimulates tissue repair

Front 2

Acute inflammation sequential order

Back 2

neutrophils
Macrophages
T cells

Front 3

Chronic inflammation

Back 3

persistent antigen can't be cleared

Front 4

What are the cells that release mediators

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1. Mast cells
2. Neutrophils
3. Macrophages
4. Eosinophils
5. T cells
6. Platelets- strictly speaking- lack nuclei

Front 5

CHEMOKINES are subset of cytokines

Back 5

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.

Front 6

What are the major groups of chemokines

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1) C-C Chemokines
2) C-X-C chemokines

according to cytosine positioning

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C-C chemokines examples:

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MIP1 alpha
MIP1 beta
Rantes
Eotaxin

aka CCLX

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CCLx

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C-C chemokines

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C-C chemokines

MEN- MTB

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secreted by macrophages, neutrophils and endothelial cells

Chemotactic for
1) macrophages
2) T and B cells

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XXC Chemokines

Back 10

iL8 trigger change of infinity in integrins

ITAC (CXCl1)
IP-10 (CXC10)

Front 11

What secretes CXC cehmokines

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Fibroblasts
Endothelial Cells
macrophages

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What are CXC's chemotactic for?

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Neutrophils
Basophils
T cells (10 and 11)

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What are CC chemokines chemotactic for?

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Macrophages
T and B cells

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What releases CC chemokines?

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Macrophages
Endothelial Cells
Neutrophils

Front 15

KININ SYSTEM

Back 15

Enzymatic cascade in plasma
Generates bradylkinin which causes

permeability, dilation, pain

REDNESS, PAIN, SWELLING

Front 16

KININ SYSTEM Symptoms

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Redness, Pain, Heat and Swelling

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Enzymatic cascade in the plasma is also known as

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CLOTTING system

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FIBRINOGEN

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converted to fibrin for converting system via THROMBIN

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FIBRIN

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makes clot and prevents blood loss

Front 20

Fibrin is chemotactic for

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NEUTROPHILS (1st response)

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Clotting system is also pro...

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Angiogenic

Angiogenesis: generation of new blood vessels

Fibrin good at simulating new blood vessel growth, for healing of wound

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Complement system as mediator

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Generates anaphylatoxins (c3a, 4a,5a)
Mast cells de-granulate = bursting of all vesicles release HISTAMINE

Front 23

Mast cells degranulation release

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HISTAMINE

Front 24

Anaphylatoxins (3a,4a,5a) are chemotactic for

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NEUTROPHILS

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What cleaves lipids?

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Macrohages
Neutrophils

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What is cleaved into protaglandins and leukotrienes

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Arachidonic acid is cleaved into pge2 and ltb4

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Pge2 and ltb4 downstream effects

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dilation, permeability, neutrophils,

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pge2 and ltb4 indirect responses?

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PAIN

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What enzyme is upstream of pge2?

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COX 1 and Cox2

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what drug is associated with Cox 1 and Cox 2?

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ADVIL

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Players for lipid mediators

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arachidonic acid
COX 1/2
pge2 and ltb4
prostalaglandins and leukotrienes

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Xox 1 web definition

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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.

Front 33

Cytokines are last mediator of inflammation

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1, 6
TNF, IFN gamma

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Neutrophils

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First cells that go to infected/damage site

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When does neutrophil influx peak

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6 hours, then thought to decline after

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Affinity of neutrophils

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10 to the 11th power

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How are neutrophils recruited?

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E and P selectin
as they express ligand for these

Front 38

What is the particular ligand Neutrophil uses to get recruited to tissue?

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PSGL-1

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Extravasation is the same except

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after entering tissue follow 83 highway
il8-3 gradient (higher concentration)

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Following 83 gradient will lead the neutrophils to

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RESPIRATORY BURST where they generate ROI: reactive oxygen intermediates

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ROI

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Reactive oxygen intermediates

Kill anything and everything around us

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What is the result of ROI?

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PUS after neutrophils explode

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Specificity of neutrophils?

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they aren't androgen specific, so they kill whatever is around.

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Accute response long mechanism

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antibodies bind to bacteria
tissue damage initiates C'(3a, 5a)
c' and mast cells

Mast cells release histamine and pge2

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accite response long mechanism 2

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endothelial cell E-selectin and neutrophil ligand (psgl1) drive migrationi nto tissue

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Acute inflammation and macrophages

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mphages will be phagocytosing bacteria and generating lipid mediators pge2

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Acute inflammation and pge2

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Affects endothelial cells
Macrophages make 1, TNF, 6

Front 48

Acute inflmmation and cytokines

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upregulated 1 TnF and 6 which regulate EC and cause neutrophil, T cells and macrophages to migrate into tissues

Front 49

What kind of gradient darw cells in

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ANAPHYLATOXINS from C' and chemokines (macrophages)

T cells- IFN gamma

Front 50

Tissue or Ec damage causes

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fibronogen to fibrin via thrombin (clotting)

Front 51

EC damage leads to

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Bradylkinin (kinin system)
permeability, dilation pain

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WHAT IS A GOOD NEGATIVE REGULATOR OF IMMUNE RESPONSE?

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TGF-beta
Stimulates tissue repair
Good to repai after you get rid of bacterial infection

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Chronic inflammation

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DTH
Unmovable antigen/stimulant

response of a lot of activated macrophages

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Chronic inflammation constantly activates

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macrophages and T cells

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Macrophage build up during Chronic inflammation

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GRANUOLA- Tuberculosis

Front 56

Chronic inflammation cells and cytokines

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macrophages and T cells
TNF and IFN gamma

Front 57

Aspirin

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irreversibly inhibits COX1
Blocks ability to generate lipid mediators

Front 58

NSAID examples

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ibuprofin, alieve, nanproxyn

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NSAIDS are good at

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reducing inflammation pain

swelling
leakage
blood flow

Reversibly inihibits COX1 (enzyme for conversion)