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Microbiology > Chapter 16: Nonspecific Immunity > Flashcards

Chapter 16: Nonspecific Immunity Flashcards

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Biology 101 flashcards
1
Q

Innate immunity

A
  • Nonspecific immunity
  • Always present and working
  • No memory/recognition of pathogens
  • Forms first two lines of defense:
    *Skin and mucous membranes
  • NK cells, phagocytes, fever, inflammation.
    -Contains and destroys most pathogens
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2
Q

Adaptive immunity

A

-Specific immunity
-Inducible
-Provides delayed responses
-Has memory/recognition on to target specific pathogens
-More powerful than innate
-Third line of defense

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3
Q

First line of defense: Barriers

A

> > Physical:
- Skin, saliva, urine flow, vomit, diarrhea, nose hairs, ciliary escalator (trachea)

> > Chemical:
-Lysozyme (sweat, tears)
-HCL and protease pepsin (stomach)
-histatin (Saliva contains antifungal)
-Sebum film that covers the body

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4
Q

Second line of defense: Immune cells, proteins, inflammation

A
  1. Neutrophils
  2. Eosinophil
  3. Basophil
  4. NK cell
  5. Macrophages
  6. Dendritic cells
    »Proteins: complement
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5
Q
  1. Neutrophils:
A

Granulocyte. First to arrive. Produces toxins to kill.
* Phagocyte. *

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6
Q
  1. Basophil:
A

Granulocyte. Signaling. Found in blood. Produced in bone marrow.
A similar cell found in tissue: Mast cell (also for signaling)

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7
Q
  1. Eosinophil:
A

Granulocyte.
Targets large pathogens (helminths) parasites.
Releases histamine.

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8
Q
  1. Natural Killer cell:
A

-Granulocyte.
Releases: Perforin, granzymes -Kills abnormal (virus infected) host (my) cells without phagocytosis or molecular recognition.

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9
Q

How to perforin and granzymes kill target cells?

A

> > Perforin: Creates holes in host cell, causing lyses

> > granzymes: apoptosis: controlled cell death

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10
Q
  1. Macrophages:
A

*Best Phagocyte.
2 types:
-Free=roams around to infection sites
-Fixed= stays in tissue
Antigen presenting cells= links to adaptive immunity

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11
Q

What cell found in the blood can become a macrophage?

A

Monocytes; they become macrophages as they enter the tissues.

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12
Q
  1. Dendritic cells:
A

*Phagocyte (eats pathogens)
Primary antigen presenting cell.
Move to immune organs.

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13
Q

Proteins: complement

A

> Activation cascade always converges at C3.
*C3–> C3A & C3B

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14
Q

Does first line innate immunity involve the activation of immune cells or proteins?

A

No, the first line of defense only used skin epithelial cells within mucus membranes. No cells or proteins.

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15
Q

Which immune cells are derived from the myeloid stem cell?

A

-Neutrophil, Eosinophil, Basophil, dendritic cells, mast cells.

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16
Q

What are TLRs?

A

Toll-like receptors.
Receptor proteins on surface of neutrophils. They recognize microbes. Signals to kills pathogen.

17
Q

PAMPS

A

Pathogen associated molecular patterns

18
Q

How are inactive complement proteins activated?

A

In response to foreign cells or lecting cause activation of C3 protein.

19
Q

Which organ produces complement proteins?

A

Liver

20
Q

What are the shorthand terms for the 2 activated complement fragments?

A

C3a and C3b

21
Q

Which specific complement protein is at the end of the activation cascade?

A

C9

22
Q

What are the three immune responses that occur after the complement activation?

A
  1. Opsonization: Coat (makes it sticky) of C3b enhances phagocytosis.
  2. Inflammation: by activating mast cells. Blood vessels become permeable and chemotactic agents attract phagocytes to area.
  3. Cytolysis: 12 C9 cells (surround) attack a microbe, making it burst.
23
Q

What is the end result when the complement cascade from C3 to C9 is completed?

A

MAC

24
Q

Which cell releases interferon alfa?

A

Virus infected cells:
-Tells neighboring cells to be more resistant to viral infection.
*proteases/nucelases to INHIBIT viruses
*AVP: antiviral proteins
-Attract NK cells to come help.

25
Q

Why are antimicrobial proteins a good defense against pathogens?

A

-Unique structural properties: 50 amino acids long.
-They’re produced when TLRs are activateed.
-Attack microbes.
-Can work together= better effectiveness.
-No known resistance by microbes.

26
Q

Five cardinal signs of inflammation:

A
  1. Pain
  2. Redness
  3. Immobility
  4. Swelling
  5. Heat
27
Q

What is the result of histamine release at the site of injury?

A
  • Increases fluid delivery
  • Vasodilation of local arteries
  • Increased permeability of blood vessels
28
Q

What is the purpose of a blood clot during inflammation?

A
  • Blocks local vessels
  • Decreases blood flow from site
  • Slows blood flow at site
  • Allows fluid to accumulate at site
29
Q

How do immune cells leave the bloodstream and travel to sites of infection?

A
  • Margination: Move to edges of vessels
  • Diapedesis: I.Cells squeeze between endothelial cells and enter tissues.
  • Chemotaxis: Immune cells travel to source of histamine. ( Neutrophils are first to arrive, then macrophages.)
30
Q

Pyrogen:

A

A chemical compound that induces fever.

31
Q

Why is a fever below 104F beneficial?

A

Fever catalyzes immune cell functions while inhibiting microbial growth.

32
Q

How does a phagocyte destroy an engulfed microorganism?

A
  1. Chemotaxis: Phagocytes follow chemical trail to site.
  2. Adherence: Phagocyte membrane attaches to foreign cell.
  3. Ingestion: Pseudopodia surround the target and fuse.
    —Engulfed target= phagosome.
  4. Digestion: Phagosome is fused with a lysosome to form the phagolysosome.
33
Q

Phagosome vs Phagolysosome

A

Phagosome: Phagocytic vesicle formed (engulfed target.)

Phagolysosome: Fusion of phagosome with lysosome.

34
Q

What is resistance?

A

Hard to kill

35
Q

What is susceptible?

A

Easy to kill

Microbiology (15 decks)

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