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POM Molecular Biology of the Cell > Inflammation > Flashcards

Inflammation Flashcards

(104 cards)

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1
Q

What are the four cardinal features of inflammation?

A

Rubor - redness
Calor - heat
Tumor - swelling
Dolor - pain

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2
Q

What causes rubor?

A

Vascular leakage leads to an accumulation of blood contents, including red blood cells which causes the redness

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3
Q

What causes calor at a site of inflammation?

A

High metabolism of infiltrating immune cells all generate heat. Also the increased presence of fluid at core body temperature at a site that usually has limited exposure

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4
Q

What is inflammation?

A

A non specific immune response to cellular injury which is designed to remove damaged cells and clear threats such as infections and pathogens
It is a complex and tightly regulated process

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5
Q

What are the causes of inflammation?

A

Pathogens, allergens, physical damage, extreme temperatures, auto-antigens, non-apoptotic cell death (necrosis and necroptosis)

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6
Q

What diseases can lead to inflammation?

A

Infection
autoimmunity
hypersensitivity
trauma
fibrotic disease
cancer

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7
Q

What cells are involved with inflammation?

A

epithelial and endothelial cells

Neutrophils
macrophages
lymphocytes
eosinophils
mast cells

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8
Q

Where can inflammation occur?

A

Any vascularised tissue

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9
Q

Is acute inflammation a fast or slow response?

A

Rapid response, non-specific response to cellular injury

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10
Q

What does acute inflammation lead to?

A

Change in local blood flow–>

Structural changes in the microvasculature–>

Recruitment/ accumulation of immune cells and proteins

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11
Q

When is inflammation initiated?

A

When cellular damage leads to the release of Damage Associated Molecular Pathogens (DAMPs) or Pathogen Associated Molecular Pathogens (PAMPs)

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12
Q

What causes swelling at a site of inflammation?

A

Vascular leakage increases blood flow into the inflamed tissue, leading to tissue buildup

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13
Q

What causes pain in an inflamed area?

A

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

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14
Q

What is meant by acute inflammation?

A

A short term process occuring in response to tissue injury, normally associated with rapid onset and resolution

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15
Q

What is acute inflammation characterised by?

A

Neutrophil recruitment

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16
Q

What triggers the release of DAMPs and PAMPs?

A

Non-apoptotic cell death eg due to a wound for example

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17
Q

What vasodilators do mast cells release?

A

Nitric oxide and histamine

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18
Q

What are the vascular changes associated with the release of histamine and nitric oxide?

A
  • Increase permeability of blood vessel wall
  • Dilation
  • Plasma leakage
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19
Q

After damage to a steady state of an organ ie., the skin, what 3 things happen?

A
  1. inflammatory signals
    - non-apoptotic cell death
    - detection of foreign material
  2. vasodilators released
    - Histamine
    - Nitric oxide
  3. vascular changes
    - increased permeability
    - dilation
    - reduced flow
    - plasma leakage
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20
Q

What 4 benefits does increased vascular permeability and leakage into an inflamed site bring? BALP

A

forms a BARRIER
more ANTIBODIES
more LEUKOCYTE migration
more PROTEINS to the site

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21
Q

What are soluble mediators released at injury?

A

Histamines, prostaglandins, cytokines (TNF, IL-1), Chemokines, Complement (C5a, C3a, C4a)

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22
Q

What are the principle sources and actions of histamines?

A

mast cells, basophils, platelets

vasodilation, increased vascular permeability, endothelial activation

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23
Q

What are the principle sources and actions of prostaglandins?

A

mast cells, leukocytes

vasodilation, pain, fever

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24
Q

What are the principle sources and actions of cytokines?

A

macrophages, endothelial cells, mast cells

endothelial activation (adhesion molecules), fever, malaise, pain, anorexia, shock

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25
What are the principle sources and actions of chemokines?
leukocytes, activated macrophages chemotaxis, leukocyte activation
26
What are the principle sources and actions of complement (C5a, C3a, C4a)?
Plasma (produced in the liver) leukocyte chemotaxis and activation, vasodilation (mast cell stimulation), opsonisation
27
Why do we experience pain during inflammation?
Due to the release of prostaglandins
28
How do neutrophils move to areas of damage?
Via chemotaxis, following a concentration gradient of chemotoxins including C5a, LTB4 and bacterial peptides
29
What is exudate?
Fluid, protein and cells that have seeped out a blood vessel
30
What does the exudate form?
A separation between healthy tissue and the inflamed tissue - acts as a physical barrier
31
What is immune cell recruitment?
- recruitment and inflammation signals at the site of damage e.g., chemokines produced - chemokines diffuse out to form a gradient - leukocytes expressing complementary chemokine receptors migrate toward the chemokine source
32
What are examples of immune cell recruitment?
Chemokine: CXCL8 otherwise known as IL-8 Receptors: CXCR1 and CXCR2, g-coupled 7-transmembrane proteins Cell type: Neutrophils. Often the first cell type recruited to the site of inflammation
33
How are neutrophils able to migrate towards the chemokine source?
They express complementary chemokine receptors which allow them to migrate towards the course
34
What is meant by neutrophil extravasation?
The movement of neutrophils from the vasculature into the surrounding tissue to reach the site of inflammation
35
What are the four steps of neutrophil extravasation?
1. Chemo-attraction 2. Rolling adhesion 3. Tight Adhesion 4. Transmigration
36
What is chemo-attraction?
Cytokines-> endothelial up-regulation of adhesion molecules e.g., selectins
37
What are the two adhesion molecules which are upregulated by cytokines?
P-selectin and E-selectin
38
How do neutrophils recognise selectin molecules on the endothelium?
They have complementary carbohydrate ligands which bind to the selectin molecules
39
What is rolling adhesion?
carbohydrate ligands in a low affinity state on neutrophils bind to selectins e.g., PSGL1 (selectin P ligand) binds P and E-selectins
40
What is the name of the P selectin ligand?
PSGL1
41
What is tight adhesion?
Chemokines promote low to high affinity switch to integrins LFA-1, Mac-1- enhance binding to ligands e.g., ICAM-1/2
42
What promotes the low to high affinity switch in integrins?
Chemokines
43
What is meant by transmigration?
Cytoskeletal re-arrangement and extension of pseudopodia. Mediated by PECAM interactions on both cells. (The movement of the neutrophil through the endothelial wall which involves the cytoskeleton of the neutrophil to be rearranged)
44
What molecule mediates the transmigration of the neutrophil molecule?
PECAM
45
What are the three functions of neutrophils at the site of inflamation?
1. Pathogen recognition 2. Pathogen clearance 3. Cytokine secretion
46
How do neutrophils recognise pathogens?
They use the TLR4 receptor and CD14 to identify lipopolysaccharides (LPS) that are present in gram negative bacteria for example
47
How do neutrophils clear pathogens?
By phagocytosis and netosis
48
What does cytokine secretion lead to?
recruitment and activation of other immune cells
49
Describe the process of phagocytosis?
1. Pathogen is engulfed into phagosome 2. Phagosome fuses with enzyme containing vesicles (lysosome) forming a phagolysosome 3. This is degraded by enzymes through acidifcation
50
What are some enzymes that could be in lysosomes?
elastase and lysozyme
51
What is released during phagocytosis which causes oxidative damage?
ROS - reactive oxygen species phagocyte NADPH oxidase antimicrobial peptides e.g., defensins
52
Give 3 reasons why the release of exudate is helpful?
Leads to increased lymphatic drainage and also allows plasma proteins like fibrin to be directly delivered to site of inflammation. Also helps to form a physical barrier between inflamed and healthy tissue
53
Why are histamine molecules turned over rapidly?
They are small molecules and therefore are rapidly degraded
54
What are the 4 resolutions of acute inflammation in the resolution phase?
1. pathogen recognition 2. short half-life 3. macrophages 4. repair/ wound healing
55
How does pathogen recognition occur?
Immune cells (e.g., neutrophils) and antimicrobials (e.g., antibodies) will recognise infections or particulates
56
Do neutrophils have a short half-life?
Yes, (especially activated)
57
What produces anti-inflammatory mediators to resolve acute inflammation? And what else do they do?
Macrophages (they also clear apoptotic cells)
58
How can acute inflammation be resolved through repair?
Infiltrating WBC clear the wound of dead cells and pathogens and release growth factors which stimulate tissue repair - ECM deposition
59
How do macrophages clear apoptotic cells?
They engulf them
60
When does chronic inflammation occur?
When the acute response cannot clear the stimuli
61
What does chronic inflammation result in?
Scarring and loss of tissue function
62
What are some diseases characterised by chronic inflammation?
Rheumatoid arthritis Asthma Inflammatory bowel disease Psoriasis Multiple sclerosis
63
What are some diseases associated with granulomatous inflammation?
Tuberculosis Leprosy Tumour reactions Foreign body granuloma
64
What are examples of persistent inflammatory stimulii?
- persistent/ prolonged infection e.g., TB, hepatitis B/C - persistent toxic stimulii e.g., allergens, pollutants - unclearable particulates e.g., silica - autoimmunity e.g., self antigens
65
What drive continual inflammation in chronic inflammation?
Antigens
66
What are the distinct cell infiltrates in chronic inflammation?
inflammatory macrophages T cells (and other lymphocytes) Plasma (antibody secreting) cells
67
Why is chronic inflammation a vicious cycle?
no clearance of inflammatory agent Bystander tissue destruction Concurrent repair processes (fibrosis and angiogenesis)
68
Why is persistent neutrophil activation bad?
It is highly toxic and leads to rapid tissue destruction
69
What is a foreign antigen?
an antigen derived from molecules not found in the body
70
What is a self antigen?
An antigen derived from molecules produced by our bodies
71
What is an immunogen?
An antigen independantly capable of driving an immune response in absence to additional substances
72
What is a hapten?
A small molecule that alone does not act as an antigen but when bound to a larger molecule it can create an antigen
73
What is granulomatous inflammation?
Chronic inflammation with distinct patterns of granuloma formation
74
How are macrophages recruited to the site of inflammation?
As monocytes, they can also be tissue residents
75
What are the benefits of macrophages being recruited to the site of inflammation?
Phagocytosis Cytotoxic Anti-inflammatory (e.g., TGF-B, IL-10) Help repair wound by building ECM
76
What are the bad things associated with macrophages being recruited to the area?
They can cause damage to healthy surrounding tissue (cytotoxic) Inflammatory Pro-fibrotic, deposit excess collagen
77
What pro-inflammatory signals do T cells release?
TNF, IL-17 and IFN-gamma
78
How do T cells promote remodelling and suppression of the immune system (aka act in a regulatory way)?
TGF-beta
79
How do T cells act in a cytotoxic manner?
through the release of perforin and granzymes
80
What do B cells do in an chronic inflammatory response?
Generate plasma cells that secrete antibodies that help to clear infection
81
Which white blood cell can act remotely during chronic inflammation?
B cells
82
What are granulomas?
Aggregation of activated macrophages
83
What triggers granuloma formation?
Strong T cell responses
84
What is the job of the granulomas?
To form a physical barrier to prevent pathogenic material from leaking out granuloma, thus allowing macrophages to clear the material
85
What is granulomatous inflammation?
(type of chronic inflammation) Inflammation with distinct pattern of granuloma formation
86
What are the differences between acute and chronic inflammation?
Acute: - Rapid onset - Lasts a few days - Vasodilation - Neutrophils predominate - Histamine release - Prominent necrosis - Scarring - Either resolved or moves on to chronic inflammation Chronic: - Delayed onset - Lasts years - Persistent inflammation - Ongoing tissue injury and attempts at healing - Monocytes and macrophages dominate - Ongoing cytokine release - Prominent scarring - Outcomes: scarring, loss of function
87
What type of cell dominates during chronic inflammation?
Monocytes / Macrophages
88
How long may a chronic inflammatory reaction last for?
Weeks, months or even years
89
What is continually released during chronic inflammation?
Cytokine release
90
What are the long term consequences of inflammation called?
The sequelae
91
What are the three possible outcomes of injury?
1. Regeneration 2. Repair / scar formation 3. Tissue scarring categorized by chronic inflammation
92
What does resolution after injury involve?
The clearance of injurious stimuli, and inflammatory mediators, replace injured cells and return to normal function
93
What does fibrosis involve as an sequalae of inflammation?
the deposition of collagen leading to excess tissue scarring and therefore the inability of the tissue to carry out its function
94
What is deposited when wounds heal?
ECM deposited
95
How do scars form?
When the collagen is unable to be removed from the site of endothelial repair
96
Why does an inflammed area become hot?
the increased presence of fluid at core body temperature at a site that would otherwise have a limited exposure to this. During inflammation infiltrating immune cells are also highly metabolically active, which may also contribute to the generation of heat as a by-product.
97
What are the positive outcomes of inflammation?
Clear inflammatory agent. Remove damaged cells Restore normal tissue function
98
What are the negative outcomes of inflammation?
Excess tissue damage Scarring Loss of organ function -> organ failure
99
What does a histopathologist do?
Deals with tissues, examines them and notes the architecture of the tissue and identify what it tells us about a particular condition
100
Describe how neutrophils are able to emigrate through the blood vessel walls?
Through the relaxation of inter-endothelial cell junctions and digestion of vascular basement membrane
101
Which chemokines released by macrophages cause chemo-attraction of neutrophils to the site of injury?
TNF and IL-1
102
Which epithelial ligand mediates transmigration of neutrophils to into the site of damage?
PECAM
103
Which chemokines cause the switch from low affinity ligands to high affinity ligands?
LFA-1 and MAC-1
104
What are the consequences of inflammation?
Broncho-pneumonia Scarring Wound healing in sensitive tissues

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