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Clinical Immunology & Viral Pathogens > Inflammation L1-2 > Flashcards

Inflammation L1-2 Flashcards

1
Q

Inflammation is an immediate response that has what 4 functions?

A
  • Restrict damage or infection to a localized area
  • Remove the causative agent and damaged tissue
  • Allow immune cells and molecules access to the site
  • Repair damaged tissue
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2
Q

Name and describe the 2 types of inflammation.

A

Acute inflammation - Initial and often transient response

Chronic Inflammation - Subsequent and often prolonged response that follows acute stages

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3
Q

Name the 5 main signs of inflammation.

A
  • Heat
  • Erytherma (Redness)
  • Oedema (Swelling)
  • Pain
  • Loss of function
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4
Q

List the 5 beneficial effects of acute inflammation.

A
  • Dilutes toxins
  • Allows entry of antibodies to site of inflammation
  • Delivers nutrients and oxygen to site of inflammation
  • Fibrin formation
  • Stimulation of the immune response
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5
Q

List the 3 harmful effects of acute inflammation.

A
  • Release of lysosomal enzymes by inflammatory cells
    may digest normal tissues
  • Swelling of acutely inflamed tissue may be harmful
  • Inappropriate inflammatory responses
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6
Q

Describe the 5 steps of acute inflammation.

A

A) Small blood vessels adjacent to the area of tissue damage become dilated with increased blood flow (VASODILATION).

B) Endothelial cells swell and partially retract so they no longer form a completely intact internal lining.

C) The vessels become leaky, allowing the passage of water, salts and some small plasma proteins into the damaged area (EXUDATION).

D) Circulating neutrophils adhere to the swollen endothelial cells (MARGINATION) and then migrate through the vessel basement membrane (EMIGRATION) passing into the area of tissue damage.

E) Small numbers of macrophages and lymphocytes migrate in a similar way as do neutrophils.

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7
Q

The activation of mast cells and subsequent release of preformed granules and synthesis of unstored mediators is believed to be central to what?

A

The development of inflammation.

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8
Q

Read:

Mast cells can be activated by a range of mediators binding to surface receptors and inducing exocytosis.

A
  1. Cross linking of IgE bound to FcεRI
  2. LPS binding to Toll Like Receptor (TLR)-4
  3. Binding of the complement breakdown products C3a and C5a to their receptors, C3AR1 and C5AR1 (CD88)
  4. CD48 binding the FimH subunit of type-1 fimbriated E.coli
  5. The neuropeptide Neuromedin U (NMU) (expressed in epidermal cells) interacts with 2 G protein coupled receptors, NMU-R1 and NMU-R2 and induces mast cells to degranulate
  6. Defensins (small cationic peptides stored in neutrophil granules - alpha defensins and epithelial cells - B defensins)
  7. Endothelins (ETs) bind to Endothelin-A Receptor
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9
Q

Which chemical mediators control vascular dilation?

A
  • Histamine
  • Prostoglandins
  • Complement components, C3a and C5a.
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10
Q

Which chemical mediators control increased vascular permeability?

A
  • Histamine
  • Kinins
  • Prostoglandins
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11
Q

Which chemical mediators control emigration of leukocytes?

A
  • C5a
  • Leukotrienes
  • IL-8,
  • Cationic proteins of neutrophils
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12
Q

What is the fluid movement across capillaries dependent on?

A

The differential pressure gradients across the vessel wall.

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13
Q

Define Oedema.

A

A condition characterized by an excess of watery fluid collecting in the cavities or tissues of the body.

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14
Q

Describe an Inflammatory Oedema.

A

An Oedema which occurs due to increased vascular permeability following tissue injury.

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15
Q

Prostoglandins, Leukotrienes and Thromboxanes are all derived from the metabolism of the long chain unsaturated fatty acid known as?

Where is it stored?

What stimulates its release?

Name the 2 pathways by which it’s metabolised.

A

Arachidonic acid.

Arachidonic acid is stored in the membranes of many cell types.

Arachidonic acid release can be initiated by a variety of stimuli including histamine and interaction of neutrophils and monocytes with damaged tissues or cells.

The Cyclo-oxygenase pathway & the 5-Lipoxygenase pathway.

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16
Q

What does the Cyclo-oxygenase metabolic pathway produce?

A

Prostoglandins and Thromboxanes.

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17
Q

Describe the individual Prostoglandins and their functions.

A
  • Prostacyclin (PGI2) inhibits platelet aggregation and causes vasodilation.
  • Stable prostoglandins (PGE2, PGF2 and PGD2) all increase vascular permeability. PGE2 also causes pain.
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18
Q

Histamine binds to one of the four major types of histamine receptors (H1 to H4).
Describe what cell type each receptor is found on.

A

H1 - Smooth Muscle and Endothelial cells
H2 - Gastric Parietal Cells
H3 - Central Nervous System
H4 - Mast Cells, Eosinophils, T cells, Dendritic Cells

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19
Q

How many types of Cyclo-oxgenase (COX) enzymes are there?

Which drugs are non-selective inhibitors of COX enzymes?

A

4.

Non steroidal anti-inflammatory drugs (NSAIDS)

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20
Q

Describe the function of Thromboxane A2.

A
  • Thromboxane A2 aggregates platelets and causes vasoconstriction.
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21
Q

What does the 5-Lipoxygenase metabolic pathway produce?

Where does the pathway occur?

A

Leukotrienes.

Mainly in neutrophils.

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22
Q

Describe the individual Leukotrienes and their functions.

A
  • LTC4, LTD and LTE4 all cause smooth muscle
    contraction and an increase in vascular permeability.
  • LTB4 stimulates the adhesion of neutrophils to
    endothelial cells and is chemotactic.
23
Q

Which cells produce TNF-alpha?

A

The main source of TNF-alpha is macrophages although it may be produced by T cells, NK cells and mast cells.

24
Q

Which cells synthesise Nitric Oxide?

Which enzyme catalyses the reaction?

What is its function?

How long is its half-life?

A
  • Endothelium and macrophages
  • Nitric Oxide Synthase
  • Nitric oxide diffuses into smooth muscle and is a potent vasodilator and increases vascular permeability
  • 3-4 seconds (very short)
25
Q

Describe cytokines.

A
  • Cytokines are small protein products of activated leukocytes, particularly lymphocytes and monocytes
  • Cytokines interact with specific receptors on target cells
- Cytokines may form a concentration gradient and are 
   therefore thought to be important controllers of directed 
  cell migration (chemotaxis)
26
Q

Name the major cytokines that play a role in inflammation.

A
  • IL-1
  • IL-8
  • TNF-alpha
27
Q

What is the principle mediator of acute inflammatory responses to gram negative bacteria and other infectious microbes?

A

TNF-alpha.

28
Q

Describe the functions of TNF-alpha.

A
  1. TNFα causes vascular endothelial to express adhesion molecules (selectins). This allows neutrophils, monocytes and lymphocytes to adhere to the endothelium prior to migration into tissues during inflammatory responses.
  2. TNFα stimulates endothelial cells to secrete chemokines that induce leukocyte chemotaxis and recruitment.
  3. TNFα stimulates macrophages to secrete IL-1.
  4. TNFα induces apoptosis in some cell types.
  5. TNFα acts on the hypothalamus to induce fever (by increased synthesis of prostoglandins by cytokine stimulated hypothalamus cells).
  6. TNFα acts on hepatocytes to increase synthesis of some serum proteins (serum amyloid A protein, fibrinogen).
29
Q

What is the principal function of IL-1?

A

IL-1 is a mediator of the host inflammatory response to infections and other inflammatory stimuli.

30
Q

Which cells produce IL-1?

Which chemicals induce its production?

A

The major source of IL-1 is macrophages.

Its production is induced by LPS and other cytokines such as TNFα.

31
Q

Name the four enzymatic cascade systems which produce various inflammatory mediators in plasma.

A
  1. The Complement system
  2. Coagulation factors system
  3. The Kinin system
  4. The Fibronolytic system
32
Q

Describe the functions of IL-1 at low and high concentrations.

A
  • At low concentrations IL-1 acts as a mediator of local inflammation (like TNFα)
  • At higher concentrations IL-1 enters the circulation and has an endocrine effect inducing fever, synthesis of acute phase proteins and initiates metabolic wasting
33
Q

What, simply, are chemokines?

A

Chemotactic cytokines.

34
Q

Which key plasma derived mediators are produced in the Coagulation factor system?

From what and how are they produced?

What do they do?

A
  • Plasmin & kallikrein
  • From plasminogen & prekallikrein
  • Both activate C5 liberating C5a. Plasmin can also cleave C3 to C3a
35
Q

How many transmembrane alpha-helical domains do all chemokine receptors have?

A

7.

36
Q

The complement system is a cascade of enzymatic proteins. It can be activated during acute inflammation in 3 ways.
Name and describe them.

A
  1. Tissue necrosis
  2. During infection - A variety of viral, bacterial, fungal and parasite material can activate complement e.g. Yeast cell walls (Zymosan), Endotoxins from Gram -ve bacteria(LPS) and polysaccharides.
  3. Products of the kinin, coagulation and fibronolytic systems.
37
Q

C3a, C4a and C5a are known as what?

What are their functions in inflammation?

A

Anaphylatoxins.

They bind to the receptors, C3aR , C4aR and C5aR and cause smooth muscle contraction and increased vascular permeability.

38
Q

Which key plasma derived mediator is produced in the Kinin system?

What does it do?

A
  • Bradykinin

- It increases vascular permeability and mediates pain.

39
Q

Which key plasma derived mediators are produced in the Fibrinolytic system?

From what and how are they produced?

What do they do?

A
  • The fibrin breakdown products; FDPX, Y, D and E
  • Plasmin is responsible for the lysis of fibrin
  • These have effects on vascular permeability
40
Q

What is the main cell to accumulate in acute inflammation during the first 24 hours following injury?

Why is it?

A
  • Neutrophil

- Due to the production of high concentrations of chemotactic factors at the site of injury (IL8 and C3a and C5a).

41
Q

What are the 3 main neutrophilic events in acute inflammation, all bought about by chemical mediators?

A
  1. The normally inactive endothelial cells are activated to allow the adhesion of neutrophils.
  2. The normally inactive circulating neutrophils are activated to enhance their capacity for phagocytosis and killing.
  3. Neutrophils develop the ability to move actively in a directional fashion from the vessels towards the site of tissue damage.
42
Q

What percentage range of white blood cells are neutrophils?

A

50-60%.

43
Q

If the tissue damage is slight there will be an adequate supply of ___1___ in the peripheral circulation.

If the tissue damage is extensive and granulocyte-stimulating factor (G-CSF) is produced stores of ___1___,
including some ___2___ forms, are released from the bone marrow. Thus there is an increased number of ___1___ in the blood.

To maintain a supply of short lived ___1___ (2 days), growth factors derived from the inflammatory process (G-CSF), stimulate the division of ___3___ precursors in the bone marrow.

A
  1. Neutrophils
  2. Immature
  3. Myeloid
44
Q

The physiological response of circulating neutrophils to chemotactic factors includes four steps.
List them.

A
  1. Margination
  2. Adherence
  3. Emigration (Extravasation)
  4. Chemotaxis
45
Q

Describe Margination.

A
  • Normally blood flows in the centre of the lumen of the
    vessel (Axial flow) whilst the area near the vessel
    wall carries only plasma (Plasmatic zone)
  • Following vasodilation the blood flow slows and
    leukocytes start to appear in the periphery of the stream
  • The result is an increase in the concentration of white
    cells adjacent to the endothelial cells in the vessel walls
46
Q

Describe Adherence.

A
  • Normally the endothelium presents a surface which
    prevents platelet aggregation and cellular migration.
  • In acute inflammation there is a change in the balance of
    many mediators
  • Thus the surface features and characteristics of both the
    endothelial cells and circulating leukocytes are altered.
  • Many cellular adhesion molecules become expressed on
    the two surfaces in response to inflammatory mediators
47
Q

Name the 2 most important adhesion molecule types in inflammation.

A
  • Intercellular adhesion molecules (ICAMS)

- Integrins

48
Q

List the 4 steps of Emigration (extravasation).

A
  1. Rolling Adhesion
  2. Tight Binding
  3. Diapedesis
  4. Migration (by chemotaxis)
49
Q

Read:

The 8 steps of Rolling Adhesion.

A
  1. The adhesive molecule P-selectin appears on the endothelial cell surface within a few minutes of exposure to histamine, C5a or LTB4.
  2. E-selectin appears a few hours after exposure to lipopolysaccharide or TNFα.
  3. These selectins recognise sialyl Lewis-X (S-Lex or CD15) on neutrophils, monocytes and eosinophils (E-selectin) and PSGL-1 on all leukocytes (P-selectin glycoprotein ligand).
  4. The interaction of P-selectin and E-selectin with S-LeX and PSGL-1 allows leukocytes to adhere and roll along the endothelium.
  5. This adhesive interaction allows the second step of
    stronger interactions to occur.
  6. PAF and C5a induce an increased expression of the
    integrins LFA-1 and CR3 and VCAM1 on leukocytes.
  7. The cytokine TNF induces the expression of the
    intracellular adhesion molecules (ICAM -1, -2 and -3)
    on endothelial cells.
  8. LFA-1 and CR-3 interact with the ICAM molecules and
    in consequence leukocytes attach firmly to the
    endothelium and the rolling stops.
50
Q

Phagocytosis is dependent upon an organised sequence of events.
List them.

A
  1. Recognition and attachment
  2. Internalisation
  3. Fusion (to form phagalosome)
  4. Digestion of internalised material
  5. Release of digested products from the cell
51
Q

What is chronic inflammation?

Why does it occur?

What does this process cause?

How do you stop it?

A

• Chronic inflammation is an inflammatory response of
prolonged duration e.g. weeks, months or indefinitely.

• The extended time course is provoked by the persistence
of the causative stimulus for the initial inflammation.

• The process causes tissue damage and is accompanied
by simultaneous attempts at healing and repair.

• Chronic inflammation will continue until the damaging
agent is removed.

52
Q

What are the 2 general features of chronic inflammation?

A
  1. A mixed cellular infiltrate which consists mainly of macrophages, lymphocytes and plasma cells (there are very few neutrophils and eosinophils).
  2. Tissue necrosis - caused by the causative agent of the
    inflammatory process.
53
Q

Describe the 3 ways accumulation of macrophages at sites of chronic inflammation occurs.

A
  1. Continued recruitment of monocytes from the circulation in response to chemotactic stimuli followed by their differentiation into macrophages in the tissue.
  2. Local proliferation of tissue macrophages.
  3. Prolonged survival and immobilisation in the inflamed area.
54
Q

Describe Granulomatous Inflammation.

A
  • Granulomatous inflammation is a histologically distinctive form of chronic inflammation.
  • A range of damaging agents can lead to the generation
    of a granuloma.
  • Granulomas are aggregates of chronic inflammatory cells
    which form small nodules < 2mm.
- Granulomas are collections of modified macrophages,
Epitheliod cells (activated macrophages), usually with a surrounding zone of lymphocytes.

Clinical Immunology & Viral Pathogens (19 decks)

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