Inflimation, Phagocytosis, Compliment System Flashcards

1
Q

Outline the inflammatory response

A

Physical barrier is broken - pathway for pathogen to enter.
Tissue resident myeloid cells act to attract more cells to site of injury/infection. Nutreophil cell numbers in blood increases. Interactions between neutrophil receptors and capillary wall slow neutrophils at site of injury/infection. Tissue resident cell signals dilate blood vessels - more blood, hotter, redder, more leaky allowing immune response into tissue. Nutreophil squeeze through leaky capillary wall and follow chemical trail to injury/infection site.

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2
Q

Are all myeloid cells phagocytic

A

No, but most are

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3
Q

Outline the 5 stages of phagocytosis

A

Phagocyte adheres to pathogens/debris. Phagocyte forms pseudopods that eventually engulf the particles, forming phagosome. Lysosome fuses with phagocytic vesicle, forming phagolysosome. Toxic compounds and lysosomal enzymes destroy pathogens. Sometimes exocytosis of the vesicles removes indigestible and residual material

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4
Q

What contents of lysosomes enable them to kill and digest phagocytoses microbes

A

Very low pH = very acidic environment (inhospitable/possibly lethal)
Reactive oxygen (hydrogen peroxide) and reactive nitrogen (nitric oxide) intermediates
Enzymes - proteases (proteins), lipases (lipids/fats), nucleuses (genetic material)

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5
Q

What is the complement cascade

A

Compliment - 9 major innate protein complexes (C1-C9) act in sequence to clear pathogens from blood and tissues. Cascade like activation. Many inactive enzymes in plasma (about 20)

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6
Q

What are the 3 functions of the complement cascade

A

Label pathogens (opsonisation)
Recruit phagocytes (chemotaxis)
Destroy pathogens (lysis)

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7
Q

What are the 3 complement pathways

A

Classical
Alternative
Lectin

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8
Q

Outline the classical complement pathway

A

If antibody has bound to the pathogen, then complement can then bind to this antibody (note: IgM is the most effective antibody isotype that can activate the classical complement pathway).

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9
Q

Outline the alternative complement pathway

A

complement binds directly to the pathogen surface or component.

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10
Q

Outline the lectin complement pathway

A

complement binds directly to carbohydrate components that are expressed on microbes.

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11
Q

Outline what is meant by complement pathways converging

A

Classical, alternative, or lectin triggers converge and result in the same amplification of C3 convertase, which results in Label, Destroy, and Recruit responses

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12
Q

What is the label outcome

A

Complement fragment C3b binds and labels the surface of the microbe, this enables phagocytes e.g. neutrophils to bind specifically to the C3b labelled microbe with its complement receptor to enhance phagocytosis.

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13
Q

What is the destroy outcome

A

Cells that are not protected by regulatory proteins are destroyed. A number of complement fragments can come together to form the MAC. This is a pore that can be formed in the bacterial cell wall causing the lysis and destruction of the microbe.

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14
Q

What is the recruitment outcome

A

C3a and C5a are both pro-inflammatory and chemoattractant to phagocytes; they can also bind to mast cells leading to their degranulation and release of further inflammatory mediators and chemoattractant molecules. Inflammation causes increased vascular permeability and ‘leaky’ blood vessels to aid the movement and recruitment of more immune cells into the area.

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15
Q

Why do membrane attack complexes not effect organisms own cells

A

Organism cells have things that inhibit perforation and phagocytosis

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