Immunbiologie B at Universität Wien | Flashcards & Summaries

Lernmaterialien für Immunbiologie B an der Universität Wien

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Septic shock vs. Toxic shock


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Septic shock: bacterial cell wall endotoxins stimulate macrophages to overproduce IL-1 and TNF-alpha
Toxic shock: Superantigen exotoxins simultaneously bind and crosslink TCRs on T-cells and MHC class 2 on APCs resulting in the antigen nonspecific stimulation of 5-25% of all T-cells. The ensuing hyperproduction of cytokines by activated T-cells causes toxic shock.

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What are toxins

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proteins.
have a very high biological activity
this biological activity can be highly specific (AB toxins) or more relaxed.
Toxins are unstable, they can be denatured by heat or acid and can be degraded by proteolytic enzymes.
Denatured toxins (toxoids) can be used as vaccines because they are not active.

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How are Exotoxins taken up?

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- food (produced in food maybe bacteria are no longer present) -> exotoxin causes symptoms and no colonization

- Exotoxin is produced at site of colonization ( wound or mucosal surface) -> acts onn tissue colonized by bacteria or enters the bloodstream

- Colonization of wound followed by local exotoxin production -> exotoxin acts locally to damage tissue or enters the bloodstream

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What do exotoxins target?

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- Cytoskeleton alteration 
- interfere with membrane associated processes in the cell (fusion/fission of vesicles)
- Cell membrane -> lysis
- Interfere with signalling processes within the cell

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Cell membrane targeting exotoxins?

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- make pores in the membrane (alpha toxin from staphylococcus)
- Target phospholipids and degrade them -> changes the property of the membrane
Or no change of phospholipid but just bind to it -> changes the properties also


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S.aureus - alpha Toxin

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Cytolytic - pore forming
small protein that forms heptameres and make pores.
changes in the conditions and homeostasis of the cell and leads to rupture and eventually inflammation.

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C. perfringens - alpha toxin

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Lipase. In gram+
cleaves phosphatidylcholin (main component of the membrane of all animal cells) -> leads to changes of the membrane and then to lysis.
High affinity to leukocytes.

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What is shock?

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A critical condition that is brought on by a sudden drop of blood flow through the body. The circulatory system fails to maintain adequate blood flow, sharply curtailing the delivery of oxygen and nutrients to vital organs. 

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Types of Exotoxins

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- cytolytic toxins (pore formin)

- AB toxins (neurotoxins, cholera, diphteria)
- superantigens

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AB toxins function

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B part docs on to the membrane, a pore is formed and the A part enters the cell.
Antibodies bind to the B part so it can not bind to the membrane.

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Clostridia Neurotoxins?
Botulinum and tetanus toxins

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AB toxins produced by spore germination.
large precursors are inactive and produced during spore germination.
They are cleaved by bacterial or tissue proteases and then internalized by receptor mediated endocytosis.
They are endopeptidases -> cleave substrates in the host cell -> located in neuro-muscular junctions.
Botulinum toxin: prevents release of acetylcholin -> muscle can not contract (BOTOX)
Tetanus toxin: inhibits inhibitory neuron -> neuron muscular junction can not be inhibited -> muscle stays contracted ->Tetanus paralyzes.

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ADP-ribosylation

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Addition od ADP-ribose to a protein. It is a reversible post-translational modification.
It is the basis for toxicity of bacterial compounds such as cholera and diptheria.

Pertussis toxin modify alpha-subunit of G-proteins which usually inhibits adenocyclase. changes the activity of the protein -> cyclase is now active all the time -> large amounts of cAMP 

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Q:
Septic shock vs. Toxic shock


A:

Septic shock: bacterial cell wall endotoxins stimulate macrophages to overproduce IL-1 and TNF-alpha
Toxic shock: Superantigen exotoxins simultaneously bind and crosslink TCRs on T-cells and MHC class 2 on APCs resulting in the antigen nonspecific stimulation of 5-25% of all T-cells. The ensuing hyperproduction of cytokines by activated T-cells causes toxic shock.

Q:

What are toxins

A:

proteins.
have a very high biological activity
this biological activity can be highly specific (AB toxins) or more relaxed.
Toxins are unstable, they can be denatured by heat or acid and can be degraded by proteolytic enzymes.
Denatured toxins (toxoids) can be used as vaccines because they are not active.

Q:

How are Exotoxins taken up?

A:

- food (produced in food maybe bacteria are no longer present) -> exotoxin causes symptoms and no colonization

- Exotoxin is produced at site of colonization ( wound or mucosal surface) -> acts onn tissue colonized by bacteria or enters the bloodstream

- Colonization of wound followed by local exotoxin production -> exotoxin acts locally to damage tissue or enters the bloodstream

Q:

What do exotoxins target?

A:

- Cytoskeleton alteration 
- interfere with membrane associated processes in the cell (fusion/fission of vesicles)
- Cell membrane -> lysis
- Interfere with signalling processes within the cell

Q:

Cell membrane targeting exotoxins?

A:

- make pores in the membrane (alpha toxin from staphylococcus)
- Target phospholipids and degrade them -> changes the property of the membrane
Or no change of phospholipid but just bind to it -> changes the properties also


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Q:

S.aureus - alpha Toxin

A:

Cytolytic - pore forming
small protein that forms heptameres and make pores.
changes in the conditions and homeostasis of the cell and leads to rupture and eventually inflammation.

Q:

C. perfringens - alpha toxin

A:

Lipase. In gram+
cleaves phosphatidylcholin (main component of the membrane of all animal cells) -> leads to changes of the membrane and then to lysis.
High affinity to leukocytes.

Q:

What is shock?

A:

A critical condition that is brought on by a sudden drop of blood flow through the body. The circulatory system fails to maintain adequate blood flow, sharply curtailing the delivery of oxygen and nutrients to vital organs. 

Q:

Types of Exotoxins

A:

- cytolytic toxins (pore formin)

- AB toxins (neurotoxins, cholera, diphteria)
- superantigens

Q:

AB toxins function

A:

B part docs on to the membrane, a pore is formed and the A part enters the cell.
Antibodies bind to the B part so it can not bind to the membrane.

Q:

Clostridia Neurotoxins?
Botulinum and tetanus toxins

A:

AB toxins produced by spore germination.
large precursors are inactive and produced during spore germination.
They are cleaved by bacterial or tissue proteases and then internalized by receptor mediated endocytosis.
They are endopeptidases -> cleave substrates in the host cell -> located in neuro-muscular junctions.
Botulinum toxin: prevents release of acetylcholin -> muscle can not contract (BOTOX)
Tetanus toxin: inhibits inhibitory neuron -> neuron muscular junction can not be inhibited -> muscle stays contracted ->Tetanus paralyzes.

Q:

ADP-ribosylation

A:

Addition od ADP-ribose to a protein. It is a reversible post-translational modification.
It is the basis for toxicity of bacterial compounds such as cholera and diptheria.

Pertussis toxin modify alpha-subunit of G-proteins which usually inhibits adenocyclase. changes the activity of the protein -> cyclase is now active all the time -> large amounts of cAMP 

Immunbiologie B

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