Lecture 14: Cationic host defence peptides Flashcards

1
Q

What is an alternative name for host defence peptides?

A

Antimicrobial peptides (AMP)

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2
Q

What is the function of AMPs?

A

To protect the host by inactivating pathogens - gram +ve, -ve, fungi, viruses- usually by disrupting the membrane.

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3
Q

What are some of the properties of AMPs?

A

Net positive charge (cationic), amphipathic to bind negative structures on membranes, produces an inflammatory response.

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4
Q

What are the two classes of AMP?

A

Cathelicidins and defensins.

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5
Q

What is the cathelicidin precursor hCAP18 broken down to form?

A

LL-37, the active peptide

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6
Q

In what cells is LL-37 stored?

A

neutrophils but also other cells such as macrophages and epithelial cells.

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7
Q

What are the important amino acid structures on defensins?

A

6 cysteines to protect from degradation by proteases, but different cysteine connectivity in the different types of defensin.

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8
Q

What are the three different classes of defensin?

A

Alpha (in the gut), beta and theta(?)

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9
Q

What gene encodes beta defensin?

A

hBD1- human B defensin 1

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10
Q

Which is the most effective antimicrobial B defensin gene?

A

hBD3

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11
Q

Where is hBD3 most commonly found?

A

In epithelial cells eg skin

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12
Q

How do AMPs work?

A

Disrupt pathogen membrane causing ions to leak out

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13
Q

Why do AMPs disrupt pathogen membranes but not host membranes?

A

Host membranes have cholesterol which protects them

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14
Q

How does LL-37 act as an immunomodulator?

A

Acts as a chemoattractant, induces histamine release, binds DNA in NETs, upreulates TLR9 and down-regulates TLR4 signalling (maybe to control immune response?)

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15
Q

How do defensins act as immunomodulators?

A

Attract DCs, mast cells, monocytes, CD4 T cells. Induce mitogenesis for wound repair.

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16
Q

What disease is linked to increased number of copies of B defensin genes?

A

Autoimmune psoriasis.

17
Q

How are B defensins implicated in psoriasis?

A

Might increase PAMP signalling to increase the innate response and contribute to inappropriate DC activation and subsequent Th1/17 activation.