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BSMS 204- Theme 1 > Lecture 2- Innate immune defences and inflammation > Flashcards

Lecture 2- Innate immune defences and inflammation Flashcards

1
Q

What is innate immunity and how fast does it react?

A

1st line of defence against infection- present at birth and passe down genetically
occurs within minutes of pathogen recognition

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2
Q

Describe the sequence of events of immediate innate immunity once the pathogen invades the tissue?

A
  • Pathogen INVADES tissue and PROLIFERATES
  • Pathogen is RECOGNISED by preformed soluble effectors and resident effector cells in the infected tissue
  • Pathogen is ELIMINATED and infection ends
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3
Q

What is the consequence if the pathogen is not eliminated by the immediate immune response?

A

ACTIVATION of cells resident in the infected tissue.
RECRUITMENT of effector cells to the infected tissue,
INFLAMMATION- fever- the acute phase response

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4
Q

Who has the conventional adaptive immunity?

A

vertebrates

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5
Q

Who has the innate immunity?

A

plants, invertebrates and vertebrates

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6
Q

What are the innate barriers to infections?

A
  1. Physical- skin, respirtaory tract and GI tract
  2. Soluble- complement, defensin and collectins
  3. Induced- innate immune cells
    PRR
    Interferons
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7
Q

What are the mechanical barriers of innate immunity in the following?
Skin, Gut, Lungs eyes, nose and oral cavity

A
  1. Skin- epithelial cells joined by tight junctions
  2. Gut longitudinal flow of fluid
  3. Lungs-mucus moved by cilia
  4. Eyes, nose, oral cavity- tears and nasal cilia
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8
Q

What happens when tissue damage occurs due to a cut of skin?

A
  1. release of VASOACTIVE and CHEMOTACTIC factors=increase blood flow and permeability
  2. permeable capillaries allow an INFLUX of fluid and cell
  3. phagocytes MIGRATE to the site if inflammation(chemotaxis)
  4. phagocytes and antibacterial exudate DESTROY the bacteria
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9
Q

Name the four types of soluble innate immunity molecules and briefly describe their function?

A
  1. Lysozymes- disrupts bacterial CELL WALL, found in blood and tears
  2. antimicrobial peptides- disrupts MICROBIAL MEMBRANE
  3. Collectins, ficolins and pentraxins- bind to pathogens targeting them for phagocytosis and ACTIVATE COMPLEMENT
  4. complement components - LYSE BACTERIA, opsonise bacteria and induce inflammation
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10
Q

Describe in detail how Lysozymes affect the bacterial cell wall and what type of cells is mostly effective against?

A

1.lysozymes secreted by- PHAGOCYTES and PANETH cells from small intestine.
2. CLEAVES the bond between the ALTERNATING sugars that make up PEPTIDOGLYCAN
B. Lysozyme effective against grams- positive bacteria

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11
Q

Which other enzyme is needed to complete the job?

A

phospholipase A2 can then disrupt the phospholipids

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12
Q

Name 3 antimicrobial peptides and describe where they are found and what type of micro-organism they are active against?

A
  1. Histatins- oral cavity and active against pathogenic funghi ( candida albicans)
  2. Cathelicidins- broad spectrum-
    active against both gram positive and negative bacteria
  3. Defensins-
    cover epithelial surfaces- found in saliva
    secreted by neutrophils, epithelia and paneth cells (from small intestine)
    Kill bacteria , fungi and viruses
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13
Q

What are the two classes of defensins? How do they act?

A

Alpha and beta defensins- AMPHIPATHIC peptides (hydrophilic and hydrophobic region)
ELECTROSTATIC attraction and the transmembrane ELECTRIC field bring the defensin into the lipid bilayer
Defensin peptides form a PORE
WATER and IONS enter
DESTROY cell

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14
Q

Describe the shape of collectins, ficolins and pentraxins and which bacterial surface do they mainly act on?

A
  1. Collectins- GLOBULAR lectin-like heads- bind bacterial CELL SURFACE sugars
  2. Ficolins- FIBROGEN like domain- recognise ACYLATED compounds which may be found in bacterial CELL WALL
  3. Pentraxins- CYCLIC MULTIMERIC proteins in plasma- CRP is an example- used clinically as a measure of inflammation- CRP binds to PHOSPHOCHOLINE on bacterial surfaces
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15
Q

How do the Collectins, ficolins and pentraxins recognise the bacteria and what process do they use to target the infect cells for phagocytosis and which pathway do they activate?

A

Collectins, ficolins and pentraxins recognise PRR-
Act as OPSONINS that bind pathogens and infected cells for phagocytosis
activate COMPLEMENT through- CLASSICAL and LECTIN pathways

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16
Q

Name the three complement pathways?

A
  1. Classical
  2. Lectin
  3. Alternative
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17
Q

How many proteins are part of the complement system that circulate in blood and tissue fluids?

A

over 30 proteins- circulate in plasma and blood

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18
Q

What happens when they detect foreign material (general detail)?

A

A CASCADE of reactions to amplify the signal

-generate inflammation and remove the pathogen

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19
Q

Where are most of these proteins made at what other cells also produce these?

A

most made at the LIVER, but also produced by MONOCYTES, MACROPHAGES and EPITHELIAL cells of the intestine and urinary tract

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20
Q

What do the complement component circulate as and what happens to them when they are activated?

A

circulated as proform- when activated they split into small and large fragments triggering amplification of cascase
e.g. C3»>C3b+C3a- normally a is the small fragment apart from C2a

21
Q

Name the FOUR effects mediated by complement components?

A
  1. bacteria Lysis
  2. Opsonization
  3. activation of inflammatory response
  4. clearance of immune complexes
22
Q

How is the classical pathway initiated?

A

initiated by C1 activation

23
Q

What three proteins make the C1 complex and what is most dominant protein?

A

C1= C1q, C1r and C1s

C1q dominates the C1 structure

24
Q

How is the Classical pathway activated and how many FC domains does C1 must bind to?

A

Activated when C1 binds to the FC region of an antibody-antigen complex
C1 must bind to at least 2 FC domains

25
Q

Which antibody is the most efficient at activating complement and why?

A

IgM- has 5 FC domains

26
Q

Which other antibodies can also activate the complement but to a lesser extent?

A

IgG1 and IgG3

27
Q

Why can’t the serum IgM bind to C1? And what causes it to allow it to bind?

A

serum IgM has planar conformation- binding antigen causes it to change shape revealing site for C1q

28
Q

What is the result of binding C1q with FC domain?

A

C1q binding with FC domain causes a CONFORMATIONAL change in C1r»>cleaving C1s

29
Q

What does the cleaved C1s activate and what are the resulting molecules?

A

Cleaved C1s activates- C2 and C4»»small and large fragments resulting in C4b2a aka C3 convertase

30
Q

What does the C3 convertase then activate and what is the result?

A

C3 convertase can activate over 200 C3 molecules- massive amplification

31
Q

What does the C4b, C2a, and C3b fragments form and what does that lead to?

A

C4b, C2a and C3b=C5 convertase&raquo_space;activating C5 leading to membrane attack complex (MAC)

32
Q

Which pathway is antibody independent and causes it to be activated?

A

Lectin pathway- activated by ficolins and mannose binding lectin (MBL)

33
Q

What is bound onto bacteria and virus in Lectin pathway?

A

MBL binds MANNOSE residue on carbohydrates and glycoproteins on bacteria and viruses

34
Q

What enzymes help to form MBL complex and what does active complex do?

A

MASP-1 and MASP-2 serine proteases - MBL complex cleaves C2 and C4

35
Q

What does C3 hydrolyse into as part of the alternative pathway?

A

C3a and C3b

36
Q

What two things does C3b bind to and what does this make it susceptible to cleavage by and what does it form?

A

C3b binds to CELL MEMBRANE and FACTOR B» making it susceptible to cleavage by FACTOR D

37
Q

What is the half-life of C3bBb? what can extend this and how?

A

C3bBb half life=5mins

By binding it to PROPEDRIN extend its half-life to 30mins- prevents its breakdown by proteases

38
Q

How can C3bBb amplify signal?

A

by hydrolysing more C3 creating more C3b amplifying the signal

39
Q

How does the membrane attack complex form?

A

C5b binds to C6 initiating the formation of MAC

40
Q

How does MAC kill the infected cell?

A

MAC forms a PORE in the membrane-

DIFFUSION of ions, small molecules and water into the cell- killing it!

41
Q

Why are the human cells not attacked by MAC?

A

Human cells have SOLUBLE and cell SURFACE associated proteins that prevents MAC formation

42
Q

What is the C1 inhibitory disease known as how does it work?

A

Heriditory angioedema - C1 inhibitor prevents C1 activating C4 and C2

43
Q

What is the result of complement deficiency?

A

recurrent infections

44
Q

What is the most severe form of complement deficiency and result?

A

C3 deficiency is the most severe- successive severe infections

45
Q

What is the consequence of C8 deficiency?

A

prone to infections with nesisseria meningitis

46
Q

What condition is associated with C4 deficiency?

A

SLE

47
Q

What is the consequence of the C4 deficiency?

A

less C3b= less C3 convertase

48
Q

What happens to C3b that is bound to immune complexes?

A

C3b bound to immune complexes binds CR1 on erythrocytes which transports them to phagocytes in the liver and spleen

49
Q

How do phagocytes recognise the immune complexes?

A

via their Fc receptors and engulf them

BSMS 204- Theme 1 (21 decks)

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