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YR 3 - Illness and Wellbeing > Immunity to Microbial Infections > Flashcards

Immunity to Microbial Infections Flashcards

1
Q

describe innate immunity

A

the first line of defence against pathogen
- general
- non-specific

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2
Q

describe adaptive immunity

A

immunity is built up from exposure and vaccinations

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3
Q

what cells are present in innate immunity?

A

phagocytes
complement cells
NK cells
lysoszymes

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4
Q

what cells are present in adaptive immunity?

A

b lymphocytes and antibodies
t lymphocytes

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5
Q

what antimicrobial factors are present within the oral cavity? (5)

A

lysozymes
antibodies - IgA, M and G
antimicrobial peptides
- defensins
- histatins
- LL37

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6
Q

what are antimicrobial peptides also known as? what are their charges?

A

host defence peptides
- all short cationic peptides - positive charge

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7
Q

where are host defence peptides produced? (3)

A
  • salivary glands
  • epithelial cells
  • leukocytes
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8
Q

4 roles of host defence peptides.

A
  • microbial activity
  • antiviral activity
  • immune cell recruitment
  • immune cell activation
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9
Q

give 3 families belonging to host defence peptides.

A

cathelicidins
defensins
histatins

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10
Q

describe defensins. the types, the composure and structure

A

2 types - alpha and beta

  • short peptides
  • 6 paired amino acid cysteine residues
  • pair up to make 3 disulfide bonds
  • structure = beta sheets - protects from overcleavage
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11
Q

how do defensins create disulfide bonds?

A

the r group on amino acid = sulfur

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12
Q

alpha defensins
- what are they produced by
- what are they known as?
- where are they stored

A

produced by neutrophils

known as human neutrophil peptides

stored in primary azurophil granules

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13
Q

how many HNP-2 are encoded by 3 alpha defensin genes?

A

3 genes
code
4 HNP

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14
Q

how can 3 genes encode 4 HNP-2?

A

3 genes
- DEFA 1
- DEFA 3
- DEFA 4

HNP-1 = DEFA1+3
HNP-2 = DEFA-4
HNP3 = combine DEFA1 or 3

HNP-1 and HNP-3 - if the N terminal is cleaved
= the same amino acid sequence as HNP-2

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15
Q

how long are HNP’s?

A

29-35 AA

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16
Q

what are HNP’s?

A

human neutrophil peptide
- alpha defensins
- host defence peptide

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17
Q

which HNPS’s are present in high abundance in the oral cavity?

A

HNP-1
HNP-2
HNP-3

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18
Q

do alpha defensins have links to periodontitis?

A

yes, there are increased levels in saliva and GCF when periodontitis are severe
- more neutrophil recruitment during perio

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19
Q

do alpha defensins have a link to edentulous patients?

A
  • there are reduced alpha defensins
  • no contact of plaque, not as much recruitment of neutrophils
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20
Q

what is neutropenia?

A

decreased levels of neutrophils

21
Q

give an example of a disease caused by neutropenia and its links to alpha defensins.

A

Morbus Kostmann
- children born without neutrophils

  • decreased levels of alpha defensins
22
Q

what 4 bacteria are alpha defensins active against?

evidence was found in vitro

A

streptococcus mutans
p gingivalis
a actinomyocytes
candida albicans

23
Q

alpha defensins regulate the immune system in three ways, explain how

A
  • HNP-1,2,3 = chemotactic for monocytes
  • draw up chemical gradient towards infection
  • increase gingival IL-8 production
  • increase cytokine expression
  • inhibit IL-10
  • increase mast cell degranulation
  • histamine released
  • vasodilation
    = neutrophil recruitment
  • activate dendritic cells
  • promote induction of adaptive immune response
24
Q

two types of defensins

A

alpha and beta

25
Q

how long are beta defensins? where are they usually produced?

A

36-45 amino acids

produced by epithelial cells
- gingival cells, salivary glands, tongue and mucosa

26
Q

what colours do alpha and beta defensins stain?

A

alpha - azure blue

beta - brown - indicates hBD-1

27
Q

describe the expression of beta defensins

A

hBD-1 - always expressed
hBD-2 - always only expressed in oral cavity, can be induced in other areas
- both expressed between layers: stratum spinosium and stratum granulosum

hBD-3 - can be induced
- expressed in stratified basal layer

hBD-4 - expressed in low levels

28
Q

describe the antimicrobial activity of beta defensions - hBD1,2,3
- level of potency
- what bacteria they are active against

A

hBD1
- least potent
- active against: p gingivalis, a actinomycetes, f nucleatum

hBD-2
- active against:
- gram negative
- candida spp

hBD-3
- most potent
- active against:
- gram negative and positive
- p gingivalis, a actinomycetes, f nucleatum, s mutans, t denticola

29
Q

how is the immune activity regulated by beta defensins?

A

hBD2,3 are activated by pro-inflam cytokines

  • activate DC and T cells
  • chemotaxis of monocytes, mast cells, T cells, dcs
30
Q

6 steps of how defensins are antiviral

A
  1. target lipid envelope
  2. extracellular aggregation
  3. receptor blocking/downregulation
  4. inhibition of binding
  5. block
  6. cellular changes
31
Q

describe the first step of defensins antiviral activity.

A
  1. targeting lipid envelope
  • defensins bind to virus
  • viral morphology changes
  • associated with reduced infectivity
32
Q

describe extracellular aggregation - 2/6 antiviral activity

A
  • virus has negative charge
  • defensins has positive charge
  • defensins clump as a result
  • can also polymerise themselves
33
Q

why is aggregation important in anti-viral activity?

A
  • body can recognise aggregated sites
  • if multiple viruses are aggregated, morphology changes, can only infect one host cell
34
Q

describe receptor blocking/downregulation - 3/6 antiviral activity

A
  • defensin can block interaction between virus and host cell receptors during the infectious stage, don’t bind together
  • host cell can become activated from the binding of defensin
  • can activate immune response/reduce no of receptors being targeted
35
Q

describe inhibition of fusion - 4/6 antiviral activity

A

defensins prevent fusion of viral nucleic acids and enzymes being delivered from the enveloped virus onto host cells

36
Q

describe blocking/uncoating - 5/6 antiviral activity

A

defensins bind to unenveloped virus - bind to the capsid

  • prevent capsid from releasing viral content
37
Q

describe the cellular changes - 6/6 antiviral activity

A
  • defensin can be detected by host cell
  • host cell change behaviour
  • viral replication requires host cell protein - PKC - protein kinase C
  • stimulated host cells from defensins can reduce the no. of proteins
    = inefficient replication
38
Q

the 3 families belonging to host defence peptides.

A

cathelicidins
defensins
histatins

39
Q

describe the structure of cathelicidins and how they differ from defensins

A

a-helical structure
- no beta sheets
- no disulfide bonds

40
Q

what is the only member of the cathelicidin family which is expressed in humans? where is it present and produced by?

A

LL37

present in saliva, salivary glands and GCF
produced by leucocytes and epithelial cells

41
Q

how does LL37 originate? How do you get it to LL37?

A

as a long peptide chain, in precursor form hCAP-18
- needs to be cleaved by proteases produced by neutrophils: Proteinase 3, Capethsin G and Neutrophil Elastase
- occurs outside of the cell
- into antimicrobial peptide

42
Q

what is the precursor for LL37 called?

A

hCAP-18

43
Q

how is LL37 stored?

A

in its precursor form - hCAP-18 in secondary granules

44
Q

link between LL37 and periodontal disease?

A

LL37 levels in GCF and saliva increase

45
Q

what bacteria is LL37 active against?

A

gram negative
- p intermedia, p gingivalis, a actinomycetes, f nucleatum

gram positive
- s gordonii, s sanguines

46
Q

how does Haim-Munk and Papillon-Lefevre Syndrome disease link to LL37?

A
  • patient will have large loss of secondary dentition
  • patients develop periodontitis due to low levels of LL37
  • due to loss of capethesin C gene
  • lack of cleaved hCAP-18 into LL37
47
Q

how does LL37 regulate the immune response? (4)

A
  1. reduces Candida albicans binding to epithelia
    - by autoaggregation
  2. promotes wound healing
    - by inhibiting inflam responses
    - neutralised gram negative
  3. stimulates pro inflam responses
    - stimulate to produce IL8
    - enhance cytokines to produce wbc
  4. chemoattractant
    - move neutrophils, T cells, mast cells, monocytes up concentration gradient
48
Q

3 models for how antimicrobial peptides damage bacterial cell membranes?

A

barrel-stave model

toroidal model - most accepted model

carpet model

49
Q

describe the toroidal model

A
  • a pore and channel made through bacterial membrane
  • lined with lipid heads and antimicrobial peptide

YR 3 - Illness and Wellbeing (31 decks)

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