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

Question 1

Complement system

Answer 1

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

Question 2

Why does the body have 3 complement systems?

Answer 2

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

Question 3

Complement: Classical pathway

Answer 3

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

Question 4

Complement: Alternative pathway

Answer 4

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

Question 5

Complement: Lectin pathway

Answer 5

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

Question 6

MAC

Answer 6

Membrane attack complex. Formed with activation of complement system.

Question 7

Which are used in Opsonizing? Inflammation? MAC?

Answer 7

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

Question 8

What is Interferon

Answer 8

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

Question 9

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

Answer 9

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

Question 10

What do interferons do?

Answer 10

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

Question 11

Mechanism of interferon (Type I)action.

Answer 11

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

Question 12

Mechanism of interferon (Type II) action.

Answer 12

Produced by activated T and NK lymphocytes; activates macrophages

Question 13

More detail, how does Interferon Type I protect?

Answer 13

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)

Question 14

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

Answer 14

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

Question 15

Interferon therapy?

Answer 15

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

Question 16

Dilation and increase permeability of blood vessels

Answer 16

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

Question 17

Degranulation of Granulocytes

Answer 17

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

Question 18

Adhesion molecules working together in diapedesis

Answer 18

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

Question 19

Prostaglandins, leukotrienes, histamines

Answer 19

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

Question 20

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

Answer 20

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

Question 21

Margination

Answer 21

Phagocytes stick to sides of blood vessels

Question 22

Chemotactic factors that are mediators of inflammation

Answer 22

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

Question 23

Pyrogens

Answer 23

Endotoxin, interleukin, interferon

Question 24

Mechanism of fever

Answer 24

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

Question 25

Benefits of fever

Answer 25

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

Question 26

Summary: Functions of innate immune system

Answer 26

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)