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Molecular Biology of The Cell - POM > Inflammation > Flashcards

Inflammation Flashcards

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1
Q

What is the characteristic pathology associated with inflammation

A

Inflammation is associated with a local higher fluid volume and higher leukocyte number

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2
Q

Why can chronic inflammation lead to tissue damage

A

Chronic inflammation can cause repetitive rounds of inflammation, tissue damage and repair that eventually result in scar formation and loss of tissue function

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3
Q

What are the five canonical signs of acute inflammation

A

Rubor (redness), tumor (swelling), calor (heat), dolor (pain) and loss of function

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4
Q

What things can cause inflammation and when is inflammation seen

A

Infection, physical tissue or cell damage, allergens, self-antigens (autoimmune disease)

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5
Q

Why does inflamed site appear red and swollen

A

As an inflammatory response, the capillaries at site of infection dilate and permeability increases, so fluid enters the tissue more easily and red because vasculature is closer to skin.

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6
Q

What are the inflammatory signals in external tissue damage

A

DAMP’s released by non-apoptotic cell death and PAMP’s by pathogens that can infect the damaged site

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7
Q

Which two vasodilator are released by mast cells in response to inflammatory signals

A

Histamine and nitric oxide

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8
Q

What are the effects in the vessels in response to vasodilators

A

The endothelial layer of the capillaries become more leaky because of bigger pores between them, causing increased vasopermeability and enlarged blood vessels. This both also reduces blood flow in capillary at inflamed site.

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9
Q

What are four benefits of increased vascular permeability and leakage in inflammation

A

Chemotaxis and easy migration for leukocytes, antibodies can enter the tissue, increased protein in tissue (for complement system), physical barrier for pathogens

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10
Q

What is the effect of prostaglandins in inflammation and which cells produce them

A

Prostaglandins are involved in vasodilation, pain and fever and are produced by mast cells and other leukocytes

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11
Q

What are complement proteins used for in inflamed tissue

A

Complement proteins can be used for opsonisation, for chemotaxis or to directly attack pathogens via MAC. It can also lead to vasodilation by activating mast cells.

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12
Q

What is exudate and what is its function in inflammation

A

Exudate is the fluid that seeps out of blood vessels with increased vascular permeability and contains fluid, proteins and leukocytes. It functions as a physical barrier for pathogens and contains all proteins and cells needed for both cellular and humoral response

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13
Q

How do leukocyte respond to chemokine gradient

A

Leukocytes move in the direction of higher complementary chemokine concentration and detect concentration by binding chemokines with complementary chemokine receptors

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14
Q

By what type of receptors binding to CXCL8 are neutrophils recruited to inflammation site

A

G-coupled transmembrane receptors complementary to IL-8

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15
Q

What is the effect of cytokines on the endothelial layer of near blood vessels

A

Cytokines stimulate cells of local endothelial layer of capillary to express adhesion molecules on cell membrane such as selectins

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16
Q

What are the four stages of neutrophil extravasation

A
  1. Chemo-attraction to inflammation site, 2. rolling adhesion to endothelial wall, 3. Tight adhesion to endothelial wall, 4. Migration through pores between endothelial cells.
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17
Q

Which ligand on neutrophil membrane is important in binding to endothelial selectins

A

Selectin binding ligands such as PSGL1 or siacyl-Lewis-X

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18
Q

Which kind of adhesion molecules is involved in the tight adhesion of neutrophils

A

Integrins expressed on neutrophil cell membrane are involved in tight adhesion of neutrophils to endothelial layer, such as LFA1 or MAC1

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19
Q

Which adhesion molecules on endothelial cells are involved in tight adhesion

A

The ICAM1 receptor on endothelial cells is involved in the tight adhesion of neutrophils to endothelial wall

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20
Q

Which molecules mediate the transmigration of the neutrophils

A

PECAM molecules on both neutrophil and endothelial cells

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21
Q

What changes intracellularly in neutrophils during transmigration

A

The cytoskeleton changes and forms pseudopodia that squeeze through pores in endothelial walls

22
Q

What are the three functions of neutrophils at the inflammation site

A

Recognising pathogen, attacking pathogen (via phagocytosis and netosis) and cytokine production

23
Q

What kind of receptors on neutrophils are used to detect lipopolysaccharides from Gram-negative bacteria

A

Toll-like receptor 4 and CD14 on neutrophil are used to detect LPS

24
Q

What is netosis and what is used for

A

Netosis is the formation of extracellular traps for pathogens, consistent of extracellullar fibres of neutrophil DNA and enzymes that break down bacterial components.

25
Q

What substances do the lysosomes involved in phagocytosis consist of

A

Lysosomes that fuse with phagosomes contain reactive oxygen species, defensins, lysozyme and elastases

26
Q

What promotes the switch from low affinity carbohydrate ligands to integrins in neutrophils

A

A high concentration of chemokines make neutrophil switch low affinity ligands to high affinity integrins for tight adhesion to endothelia vessel wall

27
Q

What is the vesicle called in phagocytosis when the phagosome and the lysosome fuse

A

Phagolysosome, which contains pathogens and enzymes that break it down

28
Q

How is the acute inflammatory response downregulated

A

Nuetrophils die very quickly after activation and inflammatory cytokines and mediators produced are very rapidly turned over

29
Q

How do macrophages downregulate the acute inflammatory response

A

Macrophages produce anti-inflammatory cytokines that inhibit neutrophil activation

30
Q

What are immunogens

A

Antigens that induce an immune response without the help of co-stimulatory or additional substances

31
Q

What are haptens

A

Antigens, usually small, that induce an immune response when they are bound to a larger molecule which is then recognised by immune system as foreign

32
Q

What is the difference between acute and chronic or granular inflammation

A

In chronic or granular inflammation there is a persistence of inflammatory stimuli and there are also inflammatory macrophages, T cells and plasma B cells infiltrated in tissue

33
Q

What is the key difference between acute and chronic inflammation

A

In chronic inflammation the inflammatory signal is not cleared and this causes a repetitious cycle of damage and repair

34
Q

What can cause persistent inflammatory stimuli

A

Resistant pathogens that fight off or evade immune response, unclearable antigens that cannot be transported away, persistant toxins or allergens that are abundant in environment, self antigens because body will continue to make these in tissues

35
Q

Which immune cells can be found in the distinct immune infiltrate in chronic inflammation

A

Inflammatory macrophages, T cells and antibody secreting plasma B cells

36
Q

What happens to the body tissues in chronic inflammation and what causes this

A

Chronic inflammation without clearance of pathogens causes bystander damage to tissue, and a repetitious cycle of damage and repair occurs that cause fibrosis and scarring of tissue and subsequently loss of tissue function

37
Q

How can fibrosis and angiogenesis occur in chronic inflammation

A

The repair of tissue damaged by bystander destruction in inflammatory response can cause formation of collagen fibres and new vasculature, when damaging process continues these collagen fibres are only thing that remains and this is fibrosis

38
Q

Why can macrophages be both good and bad in inflammation

A

Because they can be involved in both inflammatory and anti-inflammatory responses. Its cytotoxicity can be both good and bad, since it can help in an acute immune response against pathogens but also cause tissue damage in chronic inflammation. It can secrete both inflammatory and anti-inflammatory cytokines. It can help with wound repair, but this can also cause fibrosis in chronic inflammation.

39
Q

What anti-inflammatory cytokine is secreted by both macrophages and T-cells

A

TGF-β, secreted by both ant-inflammatory macrophages and regulatory T cells

40
Q

What signal from T cells induces an inflammatory response in the macrophage

A

IFN-γ, secreted by activated T cell to activate macrophage

41
Q

How can B cells affect acute and chronic inflammation remotely

A

B cells can produce antibodies in the lymph nodes which are then transported via the lymph and blood to the site of inflammation where it can bind to specific antigens

42
Q

What is granulomatous inflammation

A

Chronic inflammation of distinct location with scarring that forms a granuloma due to localised unclearable pathogen

43
Q

What is the function of the aggregation of activated macrophages in granulomas

A

The macrophages form a physical barrier to prevent pathogen from spreading

44
Q

In what situation would granulomatous inflammation occur

A

Granulomatous inflammation occurs as a response to highly resistant infectious agents such as mycobacterium or to tumours that try to evade immune response

45
Q

What can be the sequelae of acute inflammation

A

It can lead to resolution of the infection, either without damage or with abscess formation or fibrosis. It can also lead to chronic inflammation.

46
Q

What can be the sequelae of chronic inflammation

A

In can lead to progressive tissue damage that causes fibrosis and loss of function of that tissue and potentially organ.

47
Q

What is the result of chronic inflammation in tissue

A

Chronic inflammation can lead to angiogenesis, scar formation, infiltration of mononuclear leukocytes and progressive tissue damage

48
Q

What causes scarring after wounds

A

It can be difficult to remove the collagen network that has been built in wound repair process, this will leave scarring because of collagen fibres at that wound site

49
Q

How can scarring cause loss of tissue function and organ failure

A

If cells in tissue are not regenerated after damage, the collagen network cannot carry out this function and this causes loss of function of that part of the tissue or the organ itself

50
Q

What causes the heat at inflammatory site

A

In inflammation, exudate fluid originating from the blood that has a higher core temperature than superficial tissues makes superficial tissue warmer, and highly metabolically active leukocytes may add by generating heat.

51
Q

How can molecules released in acute inflammation lead to pain

A

In inflammatory response released molecules such as histamine, prostaglandins and interleukins by mast cells and neutrophils and macrophages can induce response in local nocireceptor neurone that transmits pain signals to brain.

52
Q

How can the exudate cause loss of function in alveoli

A

Exudate forms physical barrier against pathogen but can also make gas exchange in alveoli less efficient because diffusion is slowed down and this causes loss of function of lung tissue

Molecular Biology of The Cell - POM (14 decks)

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