Med Micro 4.2 - 2nd Line (comp, inf, etc) Flashcards

1
Q

Complement system

A

serum proteins. Classical pathway (dependent on ABs), Alternate Pathway (bacterial products), Lectin pathway (binds bacterial sugars). Cascade produces inflammation,

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2
Q

Why does the body have 3 complement systems?

A

Alternative: doesn’t need ABs, good for early infection.

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3
Q

Complement: Classical pathway

A

C1 binds to AB-antigen complex and becomes activated enzyme. C1 active splits C2 and C4. C4b and C2a combine, then cleave C3. C3b, C2b, and C4a combine, then cleave C5. C5b binds with C6 and C7, the C8 and many C9 attach to form MAC. C3b also acts as opsonin, C3a and C5a for chemotaxis and inflammation

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4
Q

Complement: Alternative pathway

A

Properdin factors B, P and D. Attracted to LPS, cleave C3, activate the rest. Useful in early stages in infection (don’t need ABs)

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5
Q

Complement: Lectin pathway

A

Lectins secreted by macrophages, bind to certain carbohydrates, cleave C2 and C4, activate the rest

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6
Q

MAC

A

Membrane attack complex. Formed with activation of complement system.

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7
Q

Which are used in Opsonizing? Inflammation? MAC?

A

C3a and C5a attract phagocytes and stimulate release of histamines. C3b acts as opsonin. C5b, C6, C7, C8, C9+++ in MAC

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8
Q

What is Interferon

A

Nonspecifically inhibit spread of viral infection. They are cytokines (communication) and pyrogens (muscle aches, fever). Types I (a and ß) and II (γ).

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9
Q

Type I and II interferon. What activates them? General function of each?

A

Type I induced by viral infection, Type II induced by T cells (which are induced by viral infection); Type I stimulates production of antiviral proteins early in infection, Type II stimulates phagocytic activity of macrophages and neutrophils later in infection

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10
Q

What do interferons do?

A

Activate NK, T cells, neutrophils, macrophages; up-regulate antigen presentation to T-lymphocytes; provide enhanced resistance of uninfected cells to viral attack; stimulate fever;

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11
Q

Mechanism of interferon (Type I)action.

A

transcribed etc when virus replicates in cell; interferon released and binds to another cell; new cell produces inactive antiviral proteins; virus released from original cell when it dies; virus enters new cell, genomic material activates AVP, stops protein synthesis for virus and itself. Stops the spread

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12
Q

Mechanism of interferon (Type II) action.

A

Produced by activated T and NK lymphocytes; activates macrophages

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13
Q

More detail, how does Interferon Type I protect?

A

Cells that bind interferon produce PKR, which phosphorylates eIF-2 which binds to eIF2B, which reduce protein synthesis. PKR also induces RNAse L which destroys RNA (viral and self)

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14
Q

What kind of component of the innate immune response could turn interferon on?

A

Nucleic acid of virus needs to be recognized, so the NODs could do this.

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15
Q

Interferon therapy?

A

We produce RIG-I (PRR), activates interferon regulatory factor 3 (IRF-3). Hepatitis C has protease to inhibit signal from RIG-I to IRF-3. Need to produce a protease inhibitor

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16
Q

Dilation and increase permeability of blood vessels

A

Dilation: more blood into vessels, permeability releases more fluid from blood. Blood clotting converts plasma protein to bradykinin (mediator of inflammation). Patrolling macrophages release prostaglandins and leukotrienes (response to TLR binding); basophils, platelets, and mast cells release histamine when exposed to C3a and C5a. Histamine causes dilation

17
Q

Degranulation of Granulocytes

A

C5a or C3a bind to platelets, basophils, mast cell, causes histamine release. IgE binding to an allergen has same effect

18
Q

Adhesion molecules working together in diapedesis

A

Leukocytes roll, some proteins on membrane bind to vessel wall, integrin is activated and binds even tighter.

19
Q

Prostaglandins, leukotrienes, histamines

A

All are cytokines, increase permeability and dilation of blood vessels so monocytes can do diapedesis, more antimicrobials can exit

20
Q

Summarize 9 steps of the second line in response to a cut

A
  1. Cut, bacteria in. 2. Damaged cells release histamine etc. 3. More permeability and vasodilation 4. Macrophages and neutrophils enter 5. Antimicrobials from blood, swelling 6. Blood clot 7. More phagocytes 8. Damaged tissue and leukocytes = pus 9. Stem cells rebuild
21
Q

Margination

A

Phagocytes stick to sides of blood vessels

22
Q

Chemotactic factors that are mediators of inflammation

A

Fibrin, collagen, mast cell chemotactic factors, bacterial peptides; C5a and C3a and interferon also promote vasodilation

23
Q

Pyrogens

A

Endotoxin, interleukin, interferon

24
Q

Mechanism of fever

A
  1. Pyrogens go to hypothalamus 2. Hypothalamus secretes prostaglandin which resets thermostat 3. Increase shivering, metabolic rate vasoconstriction 4. Temp raises to the reset temp
25
Q

Benefits of fever

A

Enhances the effects of interferons; Inhibits growth of some microorganisms; May enhance the performance of phagocytes, cells of specific immunity, and the process of tissue repair

26
Q

Summary: Functions of innate immune system

A

physical and chemical barrier to infectious agents; Recruiting immune cells (cytokines); complement cascade; WBC to recognize and remove foreign substances; Inflammation and Fever; Activate Adaptive (antigen presentation)