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human epithelial biology > skin microbial interactions and wound healing > Flashcards

skin microbial interactions and wound healing Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

what is the human microbiome

A

a collection of all microorganisms living in association with the human body, typically at epithelial barriers

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2
Q

how much of your body mass do microbes account for

A

1-3%

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3
Q

most microbes are either…

A

benign or beneficial

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4
Q

what do microbial skin diseases arise from

A

opportunity (eg wounding) or population imbalance

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5
Q

what are the main skin microenvironments for microbes

A
  • skin surface
  • skin glands (within the dermis)
  • gland secretions
  • damaged skin allows microbes to invade the hypodermis, subcutaneous fat layer and bloodstream where they cause serious illness
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6
Q

how many T cells are in your skin (capillaries and epidermis)

A

20 billion

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7
Q

what are the immune defenses of the skin

A
  • CD8+ T cells
  • langerhans cells
  • keratinocytes
  • dermal dendritic cells, macrophages and innate lymphoid cells (ILC)
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8
Q

how do langerhans cells protect the skin

A

they are motile dendritic immune cells in the epidermis
they are antigen presenting: phagocytose pathogens and present antigenic surface proteins to T cells

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9
Q

how do keratinocytes help protect the skin

A
  • posess toll-like receptors (TLRs)
  • detect pathogens
  • release cytokines to induce langerhans and T cell movement to site of infection
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10
Q

how do dermal dendritic cells, macrophages and ILC’s help protect the skin

A

they all conserve beneficial bacteria and attack unbeneficial bacteria
antigens presenting in dermis
ILC’s orchestrate immune responses among T cells and can suppress attack of unhelpful bacteria

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11
Q

what are the 3 phases of wound healing

A
  • inflammatory phase
  • proliferative phase
  • remodelling phase (maturation phase)
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12
Q

a brief summary of wound healing

A

keratinocytes release cytokines in inflammatory phase
bleeding clears wound and speeds up movement of macrophages in cell proliferation and matrix deposition phase
blood clot seals wound in matrix remodelling

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13
Q

what is the inflammatory phase

A

cutaneous wound = release of inflammatory cytokines which promote immune cell chemotaxis (macrophages, T cells) to site of wound. accumulation = pus

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14
Q

what is the cells of origin and function of epidermal growth factor (EGF)

A

platelets, macrophages
mitogenic for keratinocytes and fibroblasts, stimulates keratinocyte migration

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15
Q

what is the cells of origin and function of fibroblast growth factor (FGF)

A

macrophages, mast cells, T lymphocytes, endothelial cells
chemotactis and mitogenic for fibroblasts and keratinocytes, stimulates angiogenesis

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16
Q

what is the cells of origin and function of interfernon alpha, beta and gamma (IFNs)

A

lymphocytes, fibroblasts
activate macrophages, inhibit fibroblast proliferation via a feedback loop

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17
Q

what is the cells of origin and function of interleukin 1

A

macrophages, mast cells, keratinocytes, lymphocytes
induces fever and adrenocorticotropic hormone release; enhances TNF-a and IFN-y, activates granulocytes and endothelial cells; and stimulates hemotaopoiesis

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18
Q

what is the cells of origin and function of interleukin 2

A

macrophages, mast cells, keratinocytes, lymphocytes
activates macrophages, T cells, natural killer cells, and lymphokine-activated killer cells; stimulates differentiation of activates B cells; stimulates proliferation of activated B and T cells; and induces fever (increased temp = increased speed at which cells heal)

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19
Q

what is the cells of origin and function of interleukin 6

A

macrophages, mast cells, keratinocytes, lymphocytes
induces fever and enhances release of acute-phase reactants by the liver

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20
Q

what is the cells of origin and function of interleukin 8

A

macrophages, mast cells, keratinocytes, lymphocytes
enhances neutrophil adherence, chemotaxis and granule release

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21
Q

what is the cells of origin and function of keratinocyte growth factor (KGF)

A

fibroblasts
stimulates keratinocyte migration, differentiation and proliferation

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22
Q

what is the cells of origin and function of platelet-derived growth factor (PDGF)

A

platelets, macrophages, endothelial cells
cell chemotaxis, mitogenic for fibroblasts, stimulates angiogenesis, stimulates wound contraction

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23
Q

what is the cells of origin and function of transforming growth factor alpha (TGF-a)

A

macrophages, T lymphocytes, keratinocytes
mitogenic for keratinocytes and fibroblasts, stimulates keratinocyte migration

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24
Q

what is the cells of origin and function of transforming growth factor beta (TGF-b)

A

platelets, T lymphocytes, macrophages, endothelial cells, keratinocytes
cell chemotaxis stimulates angiogenesis and fibroplasia

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25
Q

what is the cells of origin and function of thromboxane A2

A

destroyed wound cell
potent vasoconstrictor

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26
Q

what is the cells of origin and function of tumour necrosis factor (TNF)

A

macrophages, mast cells, T lymphocytes
activates macrophages, mitogenic for fibroplasts, stimulates angiogenesis

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27
Q

when does the inflammatory phase occur

A

within the first 48 hours

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28
Q

when does the proliferative phase occur

A

the first 1-2 weeks

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29
Q

what happens within the proliferative phase

A
  • growth and division of epithelial cells from stratum basale (epithelialization)
  • angiogenesis in dermis
  • fibroblast proliferation in dermis deposit collagen to create supporting matrix over which the epidermal keratinocytes can grow
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30
Q

what do fibroblasts produce

A

dermal granulation tissue

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31
Q

what do tissue fibroblasts become

A

myofibroblasts induced by TGF-B1

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32
Q

when does the remodelling phase occur

A

2 weeks - months/years

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33
Q

what happens within the remodelling phase

A
  • can vary with extent of matrix deposition
  • can result in scarring as collagen type III becomes replaces by type I (which is less flexible)
  • wound may contract and increase in strength for up to 2 years after injury
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34
Q

what is remodelling

A

collagen re-organisation

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35
Q

what increases tensile strength in wounds

A

cross linking of collagen (forms homodimers with itself)

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36
Q

what are the local factors which effect wound healing

A
  • infection
  • ischemia
  • foreign bodies
  • edema / elevated tissue pressure
37
Q

what are defensins

A

antibiotic peptides produced by skin epithelial cells

38
Q

what are defensins rich in

A

cationic cysteine

39
Q

how long are defensins

A

18-45 amino acids long

40
Q

what are B-defensins a family of

A

antimicrobial peptides

41
Q

where are B-defensins secreted from

A

all epithelial cells (in skin: keratinocytes and sebaceous duct cells)

42
Q

what do defensins form part of

A

the innate immune response mechanism

43
Q

how do defensins cause lysis (degradation of cell wall)

A

permeabilize bacterial outer wall (they attack unwanted bacteria)

44
Q

an example of good skin bacteria

A

staphylococcus epidermidis

45
Q

what are the characteristics of staphylococcus epidermidis

A

gram positive, cocci, a permanent and ubiquitous coloniser of human skin

46
Q

what does staphylococcus epidermidis do for the skin

A
  • skin commensal bacterium, mostly benign
  • has mechanisms for host immune evasion
  • resists colonisation by other bacteria
  • opportunistic pathogen, will colonise material in contact with skin (eg hospital catheters), causing infection
47
Q

an example of a bad skin bacteria

A

staphylococcus aureus

48
Q

what is staphylococcus aureus

A
  • opportunistic pathogen - will colonise human skin, lung and gut
  • causes boils and abcesses
  • methicillin resistant S, Aureus (MRSA) is a major antibiotic resistant hospital pathogen
49
Q

what does staphylococcus aureus secrete

A
  • coagulase
  • hyaluronidase
  • staphylokinase
  • lipase
  • lacatamase
  • catalase
  • virulence factors
50
Q

what is coagulase

A

blood clots

51
Q

what is hyaluronidase

A

breaks down desmosomes junctions between cells

52
Q

what is staphylokinase

A

degrades fibrin and BM attachments

53
Q

what is lipase

A

degrades protective sebaceous oils

54
Q

what is lacatamase

A

degrades penicillin

55
Q

what is catalase

A

resists reactive oxygen species attack

56
Q

what do virulence factors do

A

cause rapid colonisation

57
Q

what is an example of ugly skin bacteria

A

staphylococcus aureus infection of the skin: folliculitis

58
Q

what are the characteristics of superficial folliculitis

A
  • clusters of small red or pus-filled bumps that develop around hair follicles
  • pus-filled blisters that break open and crust over
  • red and inflamed skin
  • itchiness or tenderness
59
Q

what are the characteristics of deep folliculitis

A
  • a large swollen bump or mass
  • pus-filled blisters that break open and crust over
  • pain
  • possible scars once the infection clears
60
Q

what is quorum sensing

A

homeostatic mechanism involving released peptide signals (autoinducer peptides, AIPs) that keep bacterial populations stable

61
Q

how does S, epidermidis keep S. aureus in check when beginning with a low densiting S. epidermis

A

AgrC and AgrC-P stimulate transcription factor AgrA which stimulates cell division and growth pf S. epidermidis wich results in an S. epidermidis biofilm around the base of the hair follicle

62
Q

how does S, epidermidis keep S. aureus in check when there is a low densitive mixed population of S. epidrmis and S. aureus

A

the S. epidermis AIPs dominate which causes blocakge of S. aureus AgrC and AgrA which results in A.aureus cell death. this means s. epidermis dominates and s.aureus is held in check

63
Q

what is propionibacterium acnes

A

an anaerobic bacterium found in dermal pores and hair follicles

64
Q

what is acnes nutrient source

A

sebum and shed keratin

65
Q

what is ther perfect growth condition for acne

A

elevated sebum secretion and/or follicle blockage (anaerobic and nutrient rich)

66
Q

which 3 factors contribute to sebum release rate

A

cell polarisation, cell death and cell growth

67
Q

what is sebum produced by

A

holocrine secretion

68
Q

how is sebum released from a pore

A

new cell grows around pore - other cell polarises - cell polarity = lost - cell detaches and disintegrates - contents (sebum) released into the gland lumen

69
Q

what does isotrentoin do

A

prevents acne by inhibiting sebaceous holocrine secretion

70
Q

what is the mechanism of action of isotrentoin

A

isotretinoin is made into ATRA via isomerase, which binds to RAR and RXR which binds to FoxO3a.
FoxO3a can either induce TRAIL or FoxO1
if it induces TRAIL, caspases 8 and 3 induce apoptosis and sebocyte secretion is arrested
if it induces FoxO1,p21 and p27 induce cell cycle arrest which arrests sebocyte re-growth, which unblocks the sebaceous gland lumen and so conditions are less favourable for acne growth and so inflammation subsides

71
Q

what is malassezia

A

a yeast

72
Q

how many species of malassezia are there

A

12

73
Q

what is the most common fungal commensal of human skin

A

malassezia

74
Q

where is malassezia found

A

in sebum rich areas

75
Q

what is malassezia part of

A

the normal flora of the epidermis

76
Q

what does malassezia secrete

A

phospholipase cleaving sebum lipids to inflammatory signals

77
Q

what do population imbalances of malassezia cayse

A

dandruff and seborrheic dematitis

78
Q

what does malassezia modify

A

skin epithelial cell function

79
Q

how does malassezia modify skin epithelial cell function

A
  • synthesises antibacterial compounds from skin AA’s and peptides
  • modifies keratinocyte sensitivity to UVA damage
  • inhibits melanin production
  • inhibits langerhans cell immune signalling
80
Q

where are demodex mites found

A

in hair follicles on the cheeks, nose, eyebrows, eyelashes and forehead

81
Q

what is demodex mites

A

normal skin fauna

82
Q

how long are demodex mites

A

0.1-0.4mm long

83
Q

what does over abundance of demodex mites cause

A

demodicosis and is thought to be associated with rosacea

84
Q

what is rosacea

A

inflammation and thickening of the skin

85
Q

what are erythematotelangiectatic lesions

A

irregular red lines caused by capillaries under the skin

86
Q

what are papulopustular lesions

A

small, raised pustules

87
Q

what are phymatous lesions

A

overgrowths of the sebaceous glands. lesions can occur on the forehead, eyes, nose, cheeks and chin

88
Q

what are ocular lesions

A

the skin around the eye is affected and the eye can become bloodshot (conjunctivitis)

human epithelial biology (5 decks)

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