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BIOL21351 > Lecture 3 - Acute inflammation: Main components > Flashcards

Lecture 3 - Acute inflammation: Main components Flashcards

1
Q

Acute inflammation

A

Rapid response to infection/injury (detected in minutes/hours and occurs over days)

Infections
Hypersensitivity reactions
Physical foreign bodies
Chemicals
Tissue necrosis

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2
Q

Macroscopic appearance of acute inflammation

A
  • Suppurative/purulent
  • Fibrinous
  • Pseudomembranous
  • Catarrhal
  • Haemorrhagic
  • Serous
  • Necrotising
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3
Q

Vascular characteristic signs of acute inflammation

A

Vascular events:

Celsus:
* Redness (rubor)
* Heat (calor)
* Swelling (tumor)
* Pain (dolor)

Virchow :
* Loss of function

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4
Q

Characteristic systemic events

A
  • Fever
  • loss of appetite
  • Lethargy
  • leukocytosis (increase in leukocyte number) & acute phase proteins (see later)
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5
Q

How does the host respond to inflammation?

A

Deliver leukocytes and plasma proteins to the injury/infection site for removal of necrotic tissue or pathogen:

1) Recognition of tissue damage or pathogen
* Release of chemical mediators

2) Recruitment of leukocytes and plasma proteins to the site
* Increase in blood flow and capillary permeability

3) leukocytes & plasma proteins enter tissues
* Release of chemical mediators
* phagocytosis
* Elimination of pathogen or necrotic tissue

4) repair of tissue

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6
Q

PRRs: what are they, what do they do?

A

Pattern Recognition Receptors

They mainly recognise two things:

Highly conserved structures in foreign bodies - Pathogen-associated molecular patterns (PAMPs) (e.g., lipopolysaccharide (LPS))

Danger or damage-associated molecular patterns (DAMPs) - released by injured and necrotic cells:
* intracellular proteins, proteins from ECM
* uric acid, K+, reactive oxygen species (ROS), heat-shock proteins (hsp70 and hsp90)

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7
Q

TLR: what are they, where are they found, and what do they do?

A

Toll-like receptors have 1-13 (1-10 in humans) types

Membrane-spanning proteins located in the plasma membrane & endosome

Recognise pathogens by detecting flagellin, bacterial peptidoglycans, ss/ds RNA, rRNA, profilin, diacyl/triacyl lipopeptides, unmethylated DNA, etc

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8
Q

TLR: what are they, where are they found, and what do they do?

A

Extracellular region - LRR (leucine-rich repeats) forming a horseshoe-shaped ligand binding domain

Transmembrane domain

Cytsosomal domain - toll interleukin-1

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9
Q

TLR: what are the two main responses

A

MAP kinases activated:

NF-kb activation resulting in cytokine activation and adhesion molecule expression

Interferon regulatory factors (IRFs) activating antiviral cytokines

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10
Q

What does NF-kb activation result in?

A

Pro-inflammatory kinases expression

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11
Q

What does interferon regulatory factors (IRFs) activating result in?

A

INFα and INFβ expressed - increasing viral protection

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12
Q

NOD-like receptors: what are they, what components of them are there, where are they found, how many families are there, and what do they do?

A

Nucleotide-binding oligomerisation domain receptors

A central NOD, a C-terminal LRR domain, and an N-terminal effector domain (differs between families)

In the cytoplasm

Four families: NLRA, NLRB, NLRC and NLRP - NLRB, NLRC and NLRP function in the innate immune system

Some of the members of the NLRB, NLRC and NLRP families activate inflammasomes, e.g., NLRP3

Detect PAMPs and DAMPs, activates the pro-inflammatory cytokines IL-1β and IL-18, and induce a pyroptosis

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13
Q

NLRP-3 and inflammasome complex

A

Signal 1 detected by receptor (TLRs) -> NF-kb activated, (I) Pro-IL-β and IL-18 produced

Signal 2 detected -> NLRP3, ASC, and Caspase-1 oligomerise -> Inflammasome formed -> Caspase-1 dimerises and becomes activated -> Caspase-1 activates Pro-IL-β and IL-18 -> IL-β and IL-18 are secreted

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14
Q

NLRP-3: what is its structure, what do mutations result in, and what diseases is it involved in?

A

Tripartite protein:

  • C-terminus LRR
  • Central NOD domain (NACHT)
  • N-terminus pyrid domain (PYD)

Recurrent episodes of inflammation - cryopyrin-associated periodic syndromes (CAPS)

Alzheimer’s, multiple sclerosis, Parkinson’s disease, atherosclerosis, gout, type 2 diabetes, etc.

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15
Q

ASC: what is it?

A

Adapter protein apoptosis associated speck-like protein containing a CARD

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16
Q

How powerful is IL-1β?

A

One of the most potent proinflammatory cytokines - potent endogenous pyrogen

Induces flu-like symptoms such as chills, fever, nausea, vomiting, headache and fatigue when injected into humans at 1–10 nanograms/kg of body weight

Excess production of IL-1 beta is associated with several autoimmune and inflammatory disorders

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17
Q

What two things induce VSM

A

Nitric oxide (not nitrous oxide (laughing gas)) and histamine induce Vascular Smooth Muscle

18
Q

What is the triple response to injury?

A

Red, wheal, flare

Red - vessels vasodilate for a higher blood supply

Wheal - Vessels become more permeable for more fluid release at the injury

Flare - nerve stimulation, impulse in opposing direction for opposing nerve, releasing vasodilation-inducing compounds

19
Q

What happens to fluid in the blood plasma as it travels through the capillary?

A

Beginning of capillary (arterial end):
* High hydrostatic pressure gradient (HRG)
* Low oncotic pressure gradient (OPG)
* HRG > OPG so fluid is pushed out of the capillary

End of capillary (venous end):
* Low HRG
* (relatively (~ HRG decreases while ORG remain the same)) High ORG
* ORG > HRG so fluid is drawn back in from interstitial fluid (?)

20
Q

What happens when a blood vessel has increased vascular permeability?

A

More fluid is released as well as plasma proteins and neutrophils, resulting in edema in the area

  • Caused by vessel trauma (long to repair)
  • Endothelial cell injury (short: hours – days)
21
Q

What chemical mediators cause endothelial cell contraction?

A

Histamine, bradykinin, NO, complement component C5a, LTB4, PAF, etc

22
Q

What plasma components are exudated during fluid loss from increased vascular permeability?

A

Leukocytes:
* Neutrophils (6-24 hrs) - due to the sheer amount in the plasma
* Monocytes (24-48 hrs) > macrophages

Erythrocytes (?) - dependent on size of pores

Proteins (50g/L):
* C-reactive protein (acute phase protein)
* Complement (acute phase protein, see later)
* Immunoglobulins
* Fibrinogen

23
Q

Leukocyte extravasation

A

Leukocytes may start to loosely associate with the vessel endothelial cells and may over time form stronger connections and roll along the cells until eventually passing through the cell either paracellularly (between) or transcellularly (through)

24
Q

What allows the leukocytes to roll along the endothelial cells?

A

Selectins:

L-selectins - leukocytes
E-selectins - endothelium
P-selectin - endothelium & platelets

25
Q

Sickle cell disease: what happens to selectins, what does this result in, how can this be treated, and what is the drug that treats it?

A

Upregulation of P-selectin on endothelial cells and platelets in sickle cell

Promotes binding of erythrocytes to endothelium - vaso-occlusion and sickle cell crisis

Transgenic mice with sickle cell disease and P- and E-selectin deficiencies - protected from vaso-occlusion

Crizanlizumab is a monoclonal Ab that binds to P-selectin and prevents binding to the ligand PSGL-1

26
Q

Innate immune system: specificity, what does it do, when is it used, how does it do its job, and what does it activate?

A

non-specific response to pathogens

Includes protective mechanisms, e.g., physical barriers (skin and other epithelial surfaces), mucus layers

first line of defence

components of innate immune system recognise conserved features of pathogens, e.g., viral RNA

initiates adaptive immune response

27
Q

Adaptive immune system: specificity, what does it do, how does it do its job, and why is it not the first line of defence?

A

Specific

Remembers previous encounters with specific pathogens and destroys them when they attack again and produces antibodies to destroy the pathogen

It can take time for lymphocytes (T and B cells) to become active and respond so reliant on the innate immune system in the first instance

28
Q

Cytokines: what are they, what are they produced by, what family are they a part of, what can they do, and what do they often do?

A

Small proteins secreted by cells during inflammation

Produced by many cell types but macrophages are key manufacturers

Large family of proteins which include chemokines (cytokines with chemotactic properties) and interleukins (cytokines made by one leukocyte which then acts on other leukocytes)

  • Can have autocrine, paracrine or endocrine action
  • Can be pro-inflammatory, e.g., IL-1β, IL-6 and TNF-α
  • Can be anti-inflammatory, e.g., IL-10

Often have ‘cascade’ action: one cytokine stimulates target cells to make additional cytokines: it’s complex

29
Q

Increased vascular permeability after injury: what happens?

A

The endothelial cells contract, leaving gaps and allowing plasma proteins and fluid to leave

30
Q

Predominant cell types in acute inflammation

A

Neutrophils and monocytes

31
Q

Predominant cell types in allergic reactions

A

Eosinophils

32
Q

Name two characteristic events in acute inflammation

A

Leukocytosis and increased vascular permeability

33
Q

Name 5 mediators that are responsible for increasing blood flow to an area of tissue damage or infection

A

Histamine, Bradykinin, 5-HT serotonin, prostaglandin E2, nitric oxide

34
Q

Name an example of an acute-phase protein

A

Complement C38

35
Q

What is the correct order of events in the adhesion cascade?

A

Migration, rolling, adhesion, and emigration

36
Q

Name two chemical mediators produced from arachidonic acid

A

PGI2, LTB4

37
Q

What molecules are released from damaged/necrotic cells which activate pattern recognition receptors?

A

DAMPs

38
Q

What is the role of opsonin?

A
39
Q

Which chemical mediator is directly responsible for causing fever?

A

Prostaglandin E2

40
Q

Name three drugs that can be used to slow the progress of the inflammatory disease process

A

Methotextrate, Chloroquine, Adalimumab - by injection

41
Q

Name three potential side effects of taking a non-steroidal anti-inflammatory drug (NSAID)

A

Gastric ulcers, nausea and vomiting, and renal failure

BIOL21351 (17 decks)

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