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BIOL21351 > Lecture 4 - Acute inflammation: Mediators > Flashcards

Lecture 4 - Acute inflammation: Mediators Flashcards

1
Q

Neutrophils: what do they do?

A
  • Phagocytosis
  • Generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS)
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2
Q

Monocytes: what do they do?

A
  • Phagocytosis
  • Generation of cytokines, chemokines, ROS and RNS, prostaglandins, complementary proteins, and annexin-1
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3
Q

Mast cells: what do they do?

A
  • Histamine, heparin, enzymes (tryptase, chymase), and TNF-α
  • Prostaglandins, leukotrienes, and cytokines
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4
Q

Endothelial cells: what do they do?

A
  • Release of nitric oxide
  • Expression of adhesion molecules (leukocyte binding)
  • Synthesis of prostaglandins, clotting factors, and cytokines
  • Angiogenesis in the resolution of inflammation and chronic inflammation
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5
Q

Platelets: what do they do?

A
  • Coagulation
  • Synthesis of serotonin, TXA₂, PAF, free radicals, and proinflammatory proteins
  • PDGF - repair
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6
Q

Chemical mediators: vasoactivators

A

Autacoids - substances that have a brief, localised effect in the body:
* Histamine
* Serotonin (5-HT (5-hydroxytryptamine))
* Kinins - kallikrein cleaves kininogens (pain)
* Eicosinoids

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7
Q

How do mast cells produce histamine?

A

Degranulate and form histamine

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8
Q

Where is the majority of serotonin produced?

A

Platelets

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9
Q

Eicosanoids: what are they, what are the three main ones,

A

Lipid mediators that are produced from fatty acid precursors when required and not stored preformed in cells like with histamine

Prostaglandins, thromboxanes, and leukotrienes

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10
Q

How are eicosanoids formed?

A

Phospholipase A2 gets phosphorylated and converts arachidonic acid into any of the eicosanoids

  • Cyclooxygenase will perform prostaglandins and thromboxane A2
  • Lipoxygenase will form leukotrienes
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11
Q

PGI₂

A

Prostacyclin

  • Vasodilator
  • Hyperalgesic
  • Stops platelet aggregation
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12
Q

TXA₂

A

Thromboxane A₂

  • Vasoconstrictor
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13
Q

PGF₂

A

Prostaglandin F₂

  • Bronchoconstrictor
  • Myometrial contraction
  • Vascular permeability
  • Leukocyte chemotaxis
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14
Q

PGD₂

A

Prostaglandin D₄

  • Prevent platelet aggregation
  • Vasodilator
  • Vascular permeability
  • Leukocyte chemotaxis
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15
Q

PGE₂

A

Prostaglandin E₂

  • Pyrogen - fever induced
  • Vasodilator
  • Hyperalgesic
  • Vascular permeability
  • Leukocyte chemotaxis
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16
Q

LTC₄, LTD₄, LTE₄

A

Leukotriene C₄, leukotriene D₄, and leukotriene E₄

  • Activated neutrophils
  • Generates ROS
  • Release of lysosomal enzymes
  • Bronchoconstrictors
  • Vasoconstrictors
  • Increase vascular permeability
17
Q

LTB₄

A

Leukotriene B₄

  • Chemotaxin (chemotaxis?)
  • Activate neutrophils
  • Generates ROS
  • Release of lysosomal enzymes
18
Q

Lipoxins: relation to the other eicosanoids and function

A

While the others are pro-inflammatory, lipoxins are anti-inflammatory and inhibit neutrophil chemotaxis and adhesion

19
Q

PAF: what is it, what is it produced by, and how much more effective is it than histamine?

A

Platelet-activated factor - not formed from arachidonate - not an eicosanoid (but often grouped with them)

Produced by basophils, macrophages, mast cells, neutrophils, endothelial cells, and platelets

100-10,000x more potent than histamine at inducing vasodilation and increasing vascular permeability

20
Q

TNFα: what are they produced by and what do they do?

A
  • Macrophages
  • Monocytes
  • Mast cells
  • T lymphocytes

Local effects:
* Vascular endothelium - Increased procoagulant, decreased anticoagulant, leukocyte adhesion molecule expression, and IL-1 cytokine production - Inflammation
* Leukocytes - activation, production of cytokines - Inflammation
* Fibroblasts - proliferation, collagen synthesis - Repair

Systemic effects:
* Fever - IL-6
* Leukocytosis - IL-6
* Acute phase proteins - IL-6
* Increased sleep
* Decreased appetite

21
Q

IL-1β: what are they produced by and what do they do?

A
  • Macrophages
  • Monocytes
  • endothelium
  • Dendritic cells
  • Some epithelia

Local effects:
* Vascular endothelium - Increased procoagulant, decreased anticoagulant, leukocyte adhesion molecule expression, and IL-1 cytokine production - Inflammation
* Leukocytes - activation, production of cytokines - Inflammation
* Fibroblasts - proliferation, collagen synthesis - Repair

Systemic effects:
* Fever - IL-6
* Leukocytosis - IL-6
* Acute phase proteins - IL-6
* Increased sleep
* Decreased appetite

22
Q

IL-6: what are they produced by and what do they do?

A
  • Macrophages

Systemic effects (acute phase proteins)

23
Q

Chemokines: what are they produced by and what do they do?

A

Macrophages, T lymphocytes, endothelium, and mast cells

Leukocyte recruitment

24
Q

Chemokine nomenclature

A
  • C-chemokines; one cysteine (specific for recruiting lymphocytes)
  • C-C chemokines: where there are two adjacent conserved cysteine residues
  • C-X-C chemokines: one amino acid separating the first two conserved cysteine residues - Act primarily on neutrophils to cause activation and chemotaxis of neutrophils, IL-8 is a prime example - Predominantly involved in acute inflammatory responses
  • C-XXX-C chemokines: contain three amino acids between the two cysteines
25
Q

Acute phase proteins: what causes their release, what do they cause to occur, and what do they do?

A

Release caused by interleukins, e.g., IL-1, IL-6, TNFα

  • 2-5 fold ↑: fibrinogen, mannose-binding lectin (see PRR) and complement (C3b)
  • 100-1000 fold ↑: serum amyloid, C-reactive protein (CRP)

Opsonisation: form link between microbe & phagocyte
Activation of complement cascade

26
Q

Complement cascade: what is it, what three pathways activate it, what are the major proteins, and what does it cause?

A

The body’s reaction to infection using antibodies and phagocytes to destroy microbes

Classical (C1, Antibody, Antigen), lectin (microbes + mannose-binding lectin), and alternative (LPS/endotoxin) pathways

9 major protein components: C1 – C9

activate the proteolytic cascade and links with coagulation & fibrinolytic cascade

27
Q

Complement cascade: the process

A

C3 interacts with C3 convertase, either forming C3a (resulting in inflammation, chemotaxis, and releases histamine/spasmogen)or C3b (phagocytosis - opsonin)

C3b can then form either C5a (Inflammation: chemotaxis, activates phagocytic cells, releases histamine) from C5 convertase or C5/C6/C7/C8/C9 which lyse bacteria

28
Q

Phagocytosis: the process

A
  • Microbe binds to phagocyte receptor
  • Microbe brought into the cell in a phagosome using opsonin
  • Phagosome and lysosome fuse
  • Microbe is then killed: lysosomal enzymes lyse the microbe or ROS and NO kills the microbe
29
Q

Reactive oxygen species

A

Activated by NADPH oxidase which oxidises NADPH into NADP⁺ and produces the superoxide anion (O₂*⁻) from oxygen

The superoxide can then do two different pathways to form ROS:
* Forming H₂O₂ -> myeloperoxidase causes a halide to form which reacts with H₂O₂ -> HOCl/OCl⁻ and OH*
* Nitric oxide synthase (iNOS) converts arginine into nitric oxide which forms OONO*

30
Q

ROS: what are the examples, what do they do, and how are they controlled?

A

Peroxynitrite, hydroxyl radical, hypochlorite, superoxide, and H₂O₂

Intracellular destruction of pathogens, activating chemokines, cytokines, and adhesion molecules

  • SOD: O₂*⁻ -> H₂O₂
  • Catalase: H₂O₂ -> H₂O
  • MPO: H₂O₂ -> HOCl
31
Q

NOS: what is it produced by, which is the main one in inflammation, and what

A

NO synthase (NOS) - endothelial (eNOS) and neural (nNOS)

iNOS - important in inflammation

bacterial lipopolysaccharide

cytokines

32
Q

Nitric oxide: how does it cause vasodilation,

A

It binds to the haem of guanylyl, converting GTP into cGMP which causes vasodilation

L-arginine + O₂ is catalysed by NO synthase -> L-citrulline + NO + superoxide anion (O₂*⁻) -> cytotoxic peroxynitrite anion

33
Q

Inflammatory response: Vasodilation key chemical mediators

A
  • Histamine and serotonin/5-HT
  • Kinins
  • Prostaglandins (PGI2, D2, E1 & E2)
  • NO
34
Q

Inflammatory response: Vascular permeability key chemical mediators

A
  • Histamine and serotonin/5-HT
  • NO
  • Kinins
  • C3a and C5a (indirect action by liberating vasoactive amines from mast cells)
  • Leukotrienes C4, D4, E4
35
Q

Inflammatory response: Chemotaxis, leukocyte recruitment and activation key chemical mediators

A
  • TNF, IL-1
  • Chemokines
  • C3a, C5a
  • Leukotriene B4
36
Q

Inflammatory response: Fever key chemical mediators

A
  • IL-1, TNF
  • Prostaglandins
37
Q

Inflammatory response: Pain key chemical mediators

A
  • Prostaglandins (PGI₂, E₂)
  • Bradykinin
38
Q

Inflammatory response: Tissue damage key chemical mediators

A
  • Lysosomal enzymes
  • Reactive oxygen species
  • LTB4 (indirectly via release of lysosomal enzymes)

BIOL21351 (17 decks)

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