lecture 3

Question 1

inflammatory response stage 1

Answer 1

mast cells and macrophages release chemical signals/messengers e.g cytokines or chemokines
via degranulation inflammatory responses

Question 2

damage/this causes mast cells to release….

Answer 2

Histamine- vasodilation (mediate inflammation)
Prostaglandins- vascular permeability
Leukotrienes- vascular permeability

Question 3

inflammatory response stage 2

Answer 3

more fluid into area= red, inflamed

chemotaxis- follow trail through tissue

Question 4

inflammatory response stage 3

Answer 4

phagocytosis- engulf and destroy pathogen

pus= dead neutrophils clear infection

Question 5

diapedesis process

Answer 5

process where cells and fluid leave dilated blood vessels to target area in an inflammatory response

Question 6

Type 1 interferon (Type 1 IFN) is a….

Answer 6

chemical messenger or cytokine produced by many host cell types to combat viruses
-communicate with nearby cells response
start to destroy RNA and protein synthesis (viral DNA)
or cell death to prevent viral RNA-DNA

Question 7

Toll like receptors

Answer 7

potentially disease-causing microbes recognised by innate immune cells e.g (TLR 1-9) in/on innate cells

Question 8

what do toll-like receptors bind to

Answer 8

common microbial molecular patterns
(bacterial, viral, fungal) 
e.g flagellin, lipopolysaccharide
e.g nucleic acids alter gene transcription
Leads to inflammation

Question 9

TLR engagement drives 3 innate immune mechanisms

Answer 9

phagocytosis
cytokine release
interferon release

Question 10

6 stages of phagocytosis

Answer 10

1. pseudopodia surround microbes
2. microbes adhere to phagocyte and are engulfed
3. ingestion of microbes into vacuoles ie phagosomes
4. fusion of vacuole and lysosome (phago-lysosome)
5. killing and digestion of microbe
6. elimination (exocytosis)

Question 11

killing and digesting phagocytosed microbes depends on

Answer 11

• low pH- acidic environment
• reactive oxygen (h202) and reactive nitrogen intermediates (nitric oxide)
• Enzymes: proteases, lipases, nucleases

Question 12

Triggers: 3 complement pathways

Answer 12

Classical: antibody bound to pathogen complement
Alternative: pathogen binds to complement to surface directly pathogen component
Lectin: carbohydrate components of microbes bind complement

Question 13

complement cascade how?

Answer 13

all pathways set of same cascade, inactive, cleaved, enzymatic active = amplify

Question 14

Amplification:

Answer 14

3 component pathways converge, C3 convertase (enzyme complex) otherwise susceptible to infection

Question 15

Outcomes:

Answer 15

label, destroy, recruit

Question 16

Outcome: Label

Answer 16

• Oponisation (labels pathogens which bind to complement receptors on phagocytes)
• coating microbe with antibody and/or complement fragment (C3b)

Question 17

Outcome: Recruit

Answer 17

Complement proteins act as peptide mediators of inflammation and recruit phagocytes chemotactic
release mast cells degranulated by (C3a, C5a)
inflammatory mediators released including proteins that attract phagocytes

Question 18

Outcome: Destroy

Answer 18

microbes coated with C3b are phagocytosed
Membrane attack complex (MAC) forms pores in bacterial cells= death lysis (C9)
own cells are protected by complement molecules