Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MICROM 410 > Exam 3 Lecture 26 > Flashcards

Exam 3 Lecture 26 Flashcards

1
Q

Innate immunity characteristics?

A

Evolutionarily conserved

Come from germline cells that we have at birth that encode receptors that induce antimicrobial responses

Fast-acting and non-specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How do our cells recognize a threat?

A

They see MAMPs and PAMPs

Microbiol or Pathogen Associated Molecular Patterns

These patterns are molecularly conserved in the microbial world

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Examples of a MAMP or PAMP?

A

DNA, RNA, Flagellin, Peptidoglycan, lipoteichoic acids, second messengers, LPS, fMET

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a PRR?

A

Pattern Recognition Receptor

Each one will recognize a specific MAMP or PAMP aka portion of the microbe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where are PRRs located?

A

Cell surface, in a cell compartment or in the cytosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Non-specific example of PRR?

A

TLRs

NLRs

Inflammasomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Specific Example of a PRR?

A

TLR4 located on the cell surface of macrophages, monocytes, mast cells, dendritic and intestinal epithelium.

Recognizes LPS and heat shock proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where are inflammasomes located?

A

In the cytosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is so bad about LPS?

A

Also called endotoxin and is made by gram-negative bacteria.

No Vaccine can be made

Boiling doesn’t kill

The primary cause of Gram-neg infections

Released when Gram neg bacteria die

Causes inflammation and septic shock and death in high quantities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

The main reaction to PRR?

A

Cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

True/False Some cytokines are cleaved and processed in the cytosol by inflammasomes before being released.

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are chemokines?

A

A cytokine that makes a gradient leaning neutrophils and macrophages to the infection site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Extravasation?

A

How neutrophils get fro the bloodstream to the infection site

Bradykinin and histamine are released to increase blood vessel permeability causing vasodilation.

Causes swelling and redness at infection site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Steps of extravasation?

A
  1. Cytokines activate selectins (ICAM and VCAM) on endothelial of vessel
  2. Selectins grab neutrophils and roll along the vessel
  3. Integrins bind ICAMand VCAM to the white cell/neutrophil
  4. Neutrophill squeezes through vasodilated vessel wall
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is a fever made in response to LPS or and infection?

A
  1. Monocytes activate pyrogenic cytokines that travel to the brain endothelium
  2. Elevated set point
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why fever?

A

Heat stress for invading microbes

Decreases iron availability (which microbes need)

17
Q

How do cytokines affect iron availability?

A

Decrease it by increasing production of an iron storage molecule to keep it away from invading microbes

18
Q

What happens in Septic Shock?

A

Systemic wide vasodilation which causes low blood pressure

Happens in large veins and smaller vessels

Inadequate blood flow in small vessels means organs and tissues don’t get O2

Death

19
Q

True/False Septic shock is mediated by the host and independent of the microbe

A

True

20
Q

Could injection or purified LPS or heat-killed bacteria cause Septic Shock?

A

Yes

21
Q

Other diseases caused by inflamation?

A

Autoimmune diseases such as Crohns or lung and vascular autoimmunity

22
Q

What causes a physical barrier to commensal microbes in the gut and colon?

A

Mucus protects the pits/crypts and there are stem and paneth cells at the base of the crypts/pits in gut and colon epithelium that make antimicrobial mediators

Mucus can be broken down by inflammation

23
Q

What do pathogens do if they get into the cell?

A

Disrupt actin, cytosolic delivery of ligands and enzymes, make pores, replicate, inflammasome reaction, cytokine induction cell death

Um wreak havoc and avoid host defenses to further their life Duh

24
Q

Methods they use to avoid detection?

A

Subvert- disrupt detection pathways

Host and bacteria can go back and forth- microbe subverts host figures it out and so on

Evade- mask there presence by capsule or changing the structure of MAMPs such as Y. pestis

25
Q

Types of innate immune cells that function as antigen presenting cells?

A

Any cell that has MHC on its surface can present antigens

Mainly macrophages, dendritic cells, APCs even B-Cells

T-cells and B-cell respond

26
Q

Basics of how innate immune cells work?

A

Engulfs the pathogen and places pieces of it/antigens in MHC molecule on the surface and takes it to a lymph node

T-cell recognizes antigen and activates it

T-cell activates B-cells that have seen the antigen too

B-cells generate a plasma cell that makes the antigen

27
Q

What are superantigens?

A

An antigen than doesn’t require antigen recognition to activate T-cells

Induce abnormally aggressive Tcell response and stimulate a massive amount of cytokines that lead to tissue damage and organ failure.

Toxic Shock Syndrome

28
Q

Where do superantigens bind?

A

Outside of normal antigen on the outside of MHC (APC) and TCR (T-cell) surface receptors molecules

29
Q

Example of a superantigen?

A

Staphylococcal TSST

30
Q

What do neutrophils do?

A

Innate immune cells that die when they encounter a pathogen and spill out NETS aka DNA/histones/antimicrobial compounds and innards that trap and kill bacteria

31
Q

What do Eosinophils do?

A

Innate immune cells involved in killing eukaryotic parasites

32
Q

What are monocytes?

A

Phagocytes that differentiate into macrophages and dendritic cells

33
Q

What are Mast cells and what do they do?

A

Granulocytes in connective tissue and mucosa

Have a receptor for Ige for allergic reactions

When they bind Ige they release histamine and heparin (anti-coagulant)

34
Q

Basics of how the complement system works on gram neg bacteria?

A

Causes gram neg cells to lyse

  1. IF C3b which is normally degraded encounters LPS on gram neg it binds to LPS on the exterior of bacteria and doesn’t get degraded
  2. This binding starts a C factor or complement cascade which results in the formation of a pore in the bacteria wall the MAC (membrane attack complex.
  3. Lysosome enters through the pore and degrades peptidoglycan and lyses cell
35
Q

Can the complement system lyse gram-positive bacteria?

A

No they are resistant

36
Q

2 other effects of complement factors such as C3b?

A

In addition to lysing bacteria

  1. Opsonization (initiate phagocytes)
  2. C3a and C5a are anaphylactic and induce inflammation (vasodilation, smooth muscle contractions, and histamine release)
37
Q

2 reasons complement factors induce inflammation response?

A

This is done to attract/get phagocytes to the area.

  1. This is to both kill live bacteria (phagocytosis)
  2. Clean up the dead/ already lysed bacteria
38
Q

Main ways pathogens avoid the complement system?

A
  1. Hide inside cells
  2. Make a capsule
  3. Bind host proteins that inactive complement initiators like C3b (Strep spp)
  4. Make a peptidase that breaks down C5a (Strep spp)

There are others not covered in detail on last slide

39
Q

Example of a bacteria that uses host regulatory proteins to inactivate C3b or make a peptidase to break down C5a?

A

Streptococcus spp

MICROM 410 (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions