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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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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
what is the cells of origin and function of thromboxane A2
destroyed wound cell potent vasoconstrictor
26
what is the cells of origin and function of tumour necrosis factor (TNF)
macrophages, mast cells, T lymphocytes activates macrophages, mitogenic for fibroplasts, stimulates angiogenesis
27
when does the inflammatory phase occur
within the first 48 hours
28
when does the proliferative phase occur
the first 1-2 weeks
29
what happens within the proliferative phase
- 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
30
what do fibroblasts produce
dermal granulation tissue
31
what do tissue fibroblasts become
myofibroblasts induced by TGF-B1
32
when does the remodelling phase occur
2 weeks - months/years
33
what happens within the remodelling phase
- 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
34
what is remodelling
collagen re-organisation
35
what increases tensile strength in wounds
cross linking of collagen (forms homodimers with itself)
36
what are the local factors which effect wound healing
- infection - ischemia - foreign bodies - edema / elevated tissue pressure
37
what are defensins
antibiotic peptides produced by skin epithelial cells
38
what are defensins rich in
cationic cysteine
39
how long are defensins
18-45 amino acids long
40
what are B-defensins a family of
antimicrobial peptides
41
where are B-defensins secreted from
all epithelial cells (in skin: keratinocytes and sebaceous duct cells)
42
what do defensins form part of
the innate immune response mechanism
43
how do defensins cause lysis (degradation of cell wall)
permeabilize bacterial outer wall (they attack unwanted bacteria)
44
an example of good skin bacteria
staphylococcus epidermidis
45
what are the characteristics of staphylococcus epidermidis
gram positive, cocci, a permanent and ubiquitous coloniser of human skin
46
what does staphylococcus epidermidis do for the skin
- 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
an example of a bad skin bacteria
staphylococcus aureus
48
what is staphylococcus aureus
- 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
what does staphylococcus aureus secrete
- coagulase - hyaluronidase - staphylokinase - lipase - lacatamase - catalase - virulence factors
50
what is coagulase
blood clots
51
what is hyaluronidase
breaks down desmosomes junctions between cells
52
what is staphylokinase
degrades fibrin and BM attachments
53
what is lipase
degrades protective sebaceous oils
54
what is lacatamase
degrades penicillin
55
what is catalase
resists reactive oxygen species attack
56
what do virulence factors do
cause rapid colonisation
57
what is an example of ugly skin bacteria
staphylococcus aureus infection of the skin: folliculitis
58
what are the characteristics of superficial folliculitis
- 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
what are the characteristics of deep folliculitis
- a large swollen bump or mass - pus-filled blisters that break open and crust over - pain - possible scars once the infection clears
60
what is quorum sensing
homeostatic mechanism involving released peptide signals (autoinducer peptides, AIPs) that keep bacterial populations stable
61
how does S, epidermidis keep S. aureus in check when beginning with a low densiting S. epidermis
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
how does S, epidermidis keep S. aureus in check when there is a low densitive mixed population of S. epidrmis and S. aureus
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
what is propionibacterium acnes
an anaerobic bacterium found in dermal pores and hair follicles
64
what is acnes nutrient source
sebum and shed keratin
65
what is ther perfect growth condition for acne
elevated sebum secretion and/or follicle blockage (anaerobic and nutrient rich)
66
which 3 factors contribute to sebum release rate
cell polarisation, cell death and cell growth
67
what is sebum produced by
holocrine secretion
68
how is sebum released from a pore
new cell grows around pore - other cell polarises - cell polarity = lost - cell detaches and disintegrates - contents (sebum) released into the gland lumen
69
what does isotrentoin do
prevents acne by inhibiting sebaceous holocrine secretion
70
what is the mechanism of action of isotrentoin
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
what is malassezia
a yeast
72
how many species of malassezia are there
12
73
what is the most common fungal commensal of human skin
malassezia
74
where is malassezia found
in sebum rich areas
75
what is malassezia part of
the normal flora of the epidermis
76
what does malassezia secrete
phospholipase cleaving sebum lipids to inflammatory signals
77
what do population imbalances of malassezia cayse
dandruff and seborrheic dematitis
78
what does malassezia modify
skin epithelial cell function
79
how does malassezia modify skin epithelial cell function
- synthesises antibacterial compounds from skin AA's and peptides - modifies keratinocyte sensitivity to UVA damage - inhibits melanin production - inhibits langerhans cell immune signalling
80
where are demodex mites found
in hair follicles on the cheeks, nose, eyebrows, eyelashes and forehead
81
what is demodex mites
normal skin fauna
82
how long are demodex mites
0.1-0.4mm long
83
what does over abundance of demodex mites cause
demodicosis and is thought to be associated with rosacea
84
what is rosacea
inflammation and thickening of the skin
85
what are erythematotelangiectatic lesions
irregular red lines caused by capillaries under the skin
86
what are papulopustular lesions
small, raised pustules
87
what are phymatous lesions
overgrowths of the sebaceous glands. lesions can occur on the forehead, eyes, nose, cheeks and chin
88
what are ocular lesions
the skin around the eye is affected and the eye can become bloodshot (conjunctivitis)

human epithelial biology (5 decks)

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