Host Pathogen Interactions 2

Question 1

Describe endotoxin.

Answer 1

LOS is always lacking O-antigen. LPS sometimes lacks O-antigen. Component of the outer membrane. Stimulates APCs to release cytokines

Question 2

Describe LPS structure.

Answer 2

Lipid A is the primary toxic component. Core polysaccharide is usually species specific.

Question 3

How does endotoxin cause an inflammatory response?

Answer 3

LPS shed by pathogens forms a complex with a binding protein. The complex binds to CD14 receptors and TLR4 on endothelial cells. Triggers release of cytokines and initiates adaptive immune response.

Question 4

Describe the effects of endotoxin at low concentrations.

Answer 4

Endotoxin acts as an immunostimulant. Causes release of endogenous pyrogens, activates macrophages and kinin release by neutrophils (vasodilation)

Question 5

Describe the effects of endotoxin at high concentrations.

Answer 5

Leads to hypotension and shock; Decreased cardiac output from blood pooling in tissues.

Question 6

What effect can high concentrations of endotoxin have on platelets?

Answer 6

Coagulation cascade; platelets and thrombi stick to vascular endothelium and clog small vessels. Could lead to necrosis.

Question 7

What effect can high concentrations of endotoxin have on complement?

Answer 7

Activates the alternate pathway; Production of anaphylotoxins (C3 and C4) causing vasodilation and capillary leakage.

Question 8

What are the structural categories of exotoxins?

Answer 8

AB subunit toxins, cytotoxins, and superantigens

Question 9

In AB subunit exotoxins, what is the difference between the subunits?

Answer 9

A subunit is enzymatically active (ADP-ribosyl transferase); B subunit binds to target cell. Some AB subunits act by ADP-ribosylation. ADP-ribosyl transferase takes ADP-ribose from NAD to some host molecule, causing its inactivation.

Question 10

Name the different cytolysins.

Answer 10

Phospholipases, Pore-forming toxins

Question 11

How do superantigens work?

Answer 11

They form a bridge between MHC class 2 and the TCR; Does not require processing by APCs first

Question 12

How are superantigens different from normal antigens and mitogens?

Answer 12

Mitogens stimulate all T cells to proliferate. Normal antigen activates a single or limited subset of lymphocytes. Superantigens activate a large subset of T-cells

Question 13

Whats the difference between professional and non-professional phagocytes?

Answer 13

Non-professional phagocytes are host cells that are not normally phagocytic but can be induced to do so by pathogen-specified receptor-mediated endocytosis.

Question 14

Can bacteria invade both Professional and Non-professional phagocytes?

Answer 14

Yes

Question 15

What’re the professional phagocytes?

Answer 15

Monocytes, Macrophages, neutrophils and dendritic cells.

Question 16

How do bacteria survive inside of professional phagocytes?

Answer 16

They prevent the maturation of, alter or escape the phagolysosome.

Question 17

How do bacteria survive inside of nonprofessional phagocytes?

Answer 17

They initially adhere to the host cell; Bacterial invasins bind to host cell receptors and induce uptake into host cell.

Question 18

What are the 3 mechanisms of Host cell invasion used by bacteria?

Answer 18

Trigger mechanism, Coiling phagocytosis, and zipper mechanism.

Question 19

Describe Coiling phagocytosis

Answer 19

Interaction between bacterial porin (OM protein) and complement receptor on macrophage; Coils form around organism and phagosome and sinks into cell.

Question 20

Describe the zipper mechanism.

Answer 20

Bacterial invasin binds to a host cell receptor and zips the host CM around the bacterium; Requires host cell actin network and tyrosine kinases

Question 21

Describe the trigger mechanism.

Answer 21

Bacterial type 3 secretion system injects proteins into host cell. Pathogens enters host cell surrounded by host derived membrane.