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MBC > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Define Inflammation

A

Protective biological process designed to remove damaged cells and clear threats like infections and toxins.

  • > can occur in any vascularised tissue
  • > involves not only cells at site of damage but also the recruitment of immune cells, fluid and molecular components from the circulation
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2
Q

When is it initiated?

A

When cellular damage (non-apoptotic cell death) leads to the release of damage associated molecular patterns (DAMPs)
or
body detects pathogen associated molecular patterns (PAMPs)

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3
Q

What does inflammation cause (simply put)?

A

cells in damaged tissue to secrete a range of signals designed to induce inflammation including molecules that alter the structure of nearby blood vessels and chemokines which recruit immune cells at site of injury.

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4
Q

What is the aim of immune cell recruitment?

A

To clear source of inflammatory signal and eventual resolution and repair of inflamed tissue

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5
Q

What is the characteristic pathology of inflammation?

A

Presence of increased fluid and leukocyte numbers

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6
Q

What is inflammation characterised by?

A

Acute, w/ rapid onset and resolution

Primarily characterised by recruitment of innate cells into tissue especially neutrophils

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7
Q

What happens if acute response can’t clear the stimuli?

A

Other immune cells including adaptive are recruited and it results in chronic inflammation

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8
Q

Acut v chronic

A

Acute - often resolves without any substantive damage to surrounding tissue
Chronic - repetitive rounds of inflammation, tissue damage and repair leading to scarring and loss of function

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9
Q

What kind of response to cellular injury is inflammation?

A

Non-specific, designed to remove the cause and consequence of injury. It’s also tightly regulated and complex

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10
Q

4 signs of inflammation

A
  • redness (rubor)
  • heat (calor)
  • swelling (tumor)
  • pain (dolor)
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11
Q

The stages of acute inflammation

A
  • change in local blood flow
  • structural changes in the microvasculature
  • recruitment/accumulation of immune cells and proteins
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12
Q

What type of innate cells are recruited?

A

Mast cells, neutrophils and macrophages

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13
Q

What are the vasodilators released following detection of inflammatory signals?

A

Nitric oxide

Histamine

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14
Q

What are the vascular changes?

A

Increased permeability, dilation, reduced flow and plasma leakage

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15
Q

What benefits does increased vascular permeability and leakage bring?

A

More antibodies, proteins (increased activation of immune system’s tissue repair), a bigger barrier to healthy tissues, higher leukocyte migration

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16
Q

List the soluble mediators, their sources and their actions when released at an injury (5)

A
  • Histamine - mast cells, basophils, platelets -> vasodilation, increased vascular permeability, endothelial activation
  • Prostaglandins - mast cells, leukocytes -> vasodilation, pain, fever
  • Cytokines (TNF, IL-1) - macrophages, endothelial cells and mast cells -> endothelial activation (adhesion molecules), fever, malaise, pain, anorexia, shock
  • Chemokines - leukocytes, activated macrophages -> chemotaxis, leukocyte activation
  • Complement (C5a, C3a, C4a) - plasma (produced in liver) -> leukocyte chemotaxis and activation, vasodilation (mast cell stimulation), opsonisation
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17
Q

What is exudate and what is its function?

A

Fluid, proteins and cells that have seeped out of a blood vessel which form a barrie inbetween inflamed tissue and healthy tissue

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18
Q

What cell is recruited first?

A

neutrophils

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19
Q

How does chemotaxis happen?

A

Chemokines diffuse out to form a gradient and leukocytes expressing complementary receptors migrate toward the chemokine source.

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20
Q

Explain neutrophil extravasation

A
  1. Chemo-attraction - cytokines -> endothelial upregulation of adhesion molecules - selectins
  2. Rolling adhesion - carbohydrate ligands in a low affinity state on neutrophils bind selectins (e.g. PSGL1 binds P and E-selectins)
  3. Tight adhesion - chemokines promote low to high affinity switch in integrin LFA-1, Mac-1 - enhance binding to ligands e.g. ICAM-1/2
  4. Transmigration - Cytoskeletal rearrangement and extension of pseudopodia mediated by PECAM interactions on both cells.
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21
Q

Neutrophil function at the site of inflammation

A
  1. Pathogen recognition - use of TLR4 and CD14 to identify the lipopolysaccharides (LPS) present in gram-negative bacteria
  2. Pathogen clearance - phagocytosis and netosis (neutrophil extracellular death)
  3. Cytokine secretion - recruitment and activation of other immune cells
22
Q

Explain phagocytosis

A
  • large particles engulfed into membrane bound vesicles (phagosome)
  • Phagosome fuses with lysosome (vesicles containing enzymes e.g. elastase and lysozyme) -> phagolysosome
  • reactive oxygen species (ROS) - phagocyte NADPH oxidase
  • antimicrobial peptides - e.g. defensins
23
Q

Explain the resolution of acute inflammation

A
  1. Pathogen recognition
  2. Short half life - Neutrophils (especially activated) have a rapid half-life; inflammatory mediators are turned over rapidly
  3. Macrophages - Clear apoptotic cells and produce anti-inflammatory mediators
24
Q

What is an immunogen?

A

An antigen independently capable of driving an immune response in the absence of additional substances

25
Q

What is a hapten?

A

A small molecule that alone does not act as an antigen but when bound to a larger molecule it can create an antigen

26
Q

Definition of an antigen

A

A molecule or molecular structure that can be recognised by an antibody

any substance to which your immune system can mount an antibody or adaptive immune response

27
Q

Some diseases characterized by chronic inflammation

A 
Rheumatoid arthritis
Asthma 
Inflammatory bowel syndrome 
Glomerulonephritis 
Hepatitis 
Psoriasis
Multiple sclerosis
28
Q

Diseases associated with granulomatous inflammation

A 
TB 
leprosy
foreign body granuloma
tumour reactions 
Sarcoidosis 
Crohn's disease
29
Q

Characteristics of chronic inflammation

A

Similar but very different to acute inflammation

Persistent inflammatory stimuli - persistent prolonged infection (TB, hep B/C); persistent toxic stimuli; unclearable particulates e.g. silica; Autoimmunity e.g. self antigens

Distinct immune cell infiltrate - Inflammatory macrophages, T cells (and other lymphocytes), plasma (antibody secreting) cells

A vicious cycle - no clearance, bystander tissue destruction, concurrent repair processes (fibrosis and angiogenesis)

30
Q

How can macrophages be recruited?

A

Can be recruited as monocytes to site of inflammation but there are also tissue resident macrophages

31
Q

Benefits v Negatives of macrophages

A

Benefits:

  • Phagocytic
  • Cytotoxic
  • Anti-inflammatory (e.g. TGF beta, IL-10)
  • Wound repair (TGF beta, PDGF, FGF)

Negatives:
- Cytotoxic, inflammatory, pro-fibrotic

32
Q

Role of T cells in inflammation

A

pro-inflammatory (TNF, IL-17, IFN-gamma)

cytotoxic (granzymes, perforin)

Regulatory (e.g. TGF-beta (promotes remodelling and suppression of the immune system))

33
Q

What is granulomatous inflammation?

A

Chronic inflammation with distinct pattern of granuloma formation (and tissue scarring)

34
Q

What is granulomatous inflammation triggered by?

A

strong T-cell responses and resistant agents

35
Q

What is the purpose of a barrier designed for clearance and aggregated macrophages?

A

Prevent leakage out of site and help the macrophages clear the infection.

36
Q

What is the predominant immune cell in acute vs chronic inflammation?

A

Neutrophils (acute)

Monocytes/Macrophages (chronic)

37
Q

What is the most abundant soluble mediator in acute vs chronic inflammation?

A

Histamine (acute)

Ongoing cytokine release (chronic)

38
Q

Vital signs in acute vs chronic?

A

Prominent necrosis (acute)

Prominent scarring (chronic)

39
Q

Outcomes of acute inflammation?

A

Complete resolution
or
Progression to Chronic Inflammation

40
Q

Outcomes of chronic inflammation?

A

Scarring
or
Loss of function

41
Q

What is pus formation a sign of?

A

Acute inflammation

It is also called abscess and it is formed when there may be a need to repair vasculature => fibrosis occurs

42
Q

What does sequalae mean?

A

Consequences of

43
Q

What is wound healing?

A

Extracellular matrix deposition (e.g. collagen)

44
Q

How and why does vasodilation occur in inflammation?

A

Due to mast cell derived histamine and nitric oxide on the vascular endothelium the tight junctions break down which promotes vascular leakage and increased blood flow

45
Q

Why do we feel heat at the site of injury?

A

Due to increased presence of fluid at core body temperature at a site that otherwise wouldn’t be exposed to it; plus infiltrating immune cells are highly metabolically active

46
Q

Why do we feel pain?

A

Many of the mediators that signal to endothelial cells and other immune cells during inflammation also signal to local nerve cells

47
Q

What is the 5th cardinal feature of inflammation?

A

Functio laesa (loss of function)

48
Q

What are parenchymal cells?

A

These are the cells that perform the biological function of organs (e.g. the cells in the alveoli in the lungs)

49
Q

How are neutrophils slowed down in the blood stream?

A

Via the formation of transient bonds between Sialayl Lewis X (carbohydrate on neutrophils) and selectins

50
Q

Why do neutrophils have a rolling adhesion?

A

They roll due to the blood flow

51
Q

What specifically happens during tight adhesion?

A

Via integrins (LFA1) on neutrophil undergo conformational change and bind to ICAM1 molecules on the endothelial wall making diapedesis (process of squeezing out) begin

MBC (3 decks)

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