Practice development


rather like cement in a wall. These lipids also repel water while their acidic pH is hostile to bacteria (normal tissue pH is 7.4 while on the surface of the skin the pH is 6.5).


Rigid cytoskeleton


Figure 2 – Terminal differentiation. Intercellular cornified envelope


Page points


1. The uppermost viable cell layer is held firmly together by a complex of small cell surface membrane proteins


2. While the skin barrier is hostile to most bacteria, some species are able to


survive, for example Staphylococcus epidermidis and the coryneform bacteria Propionibacterium acnes


3. When the normal skin barrier is breached the dynamics of the


host response to the environment are drastically changed to favour colonisation by microbes


4. Thus rapid wound healing is


essential to protect the host from the environment


are programmed to terminally differentiate and no longer proliferate. These terminally differentiated (committed) keratinocytes undergo epigenetic changes that set them apart from cells in the basal layer. Consistent with the process of terminal differentiation, keratinocytes in the basal layer change their cytoskeletal protein (keratin intermediate filament) expression pattern as they move into the suprabasal layer, in contrast to the basal keratins (these are rigid and contribute to the structural integrity of the skin in the same way that the bony skeleton provides support and integrity to the rest of the body). As the committed keratinocytes are pushed


further up the epidermis, multiple small proteins are secreted that collapse and harden their cell membrane (termed the cornified envelope [Fig 2]), so that the surface keratinocytes become similar to bricks in a wall. Thus the skin epidermis forms a hardened barrier to the environment, which is dependent upon this highly regulated process of terminal differentiation.


References


1. Irwin McLean WH. The allergy gene. The Scientist 2010; 24: 34.


2. Patel GK, Llewellyn M, Harding


KG. Managing gravitational eczema and allergic contact dermatitis. Br J Comm Nurs 2001; 6: 394–406.


3.World Union of Wound Healing Societies (WUWHS). Compression in Venous Leg Ulcers: a consensus document. 2008; MEP Ltd, London.


FORMATION OF TIGHT JUNCTIONS The uppermost viable cell layer is held firmly together by a complex of small cell surface membrane proteins. These proteins form bonds called tight junctions [Fig 3], which hold the keratinocytes at this layer together so tightly that they prevent water from leaking out of the skin and microbes from entering.


LIPIDS In addition to the multiple small proteins that are released near the skin surface to form the cornified envelope (as discussed above), small fatty acids are also released into the extracellular space in the upper layers of the skin. These lipids [Fig 4] surround and fix the brick-like keratinocytes on the skin’s surface,


15 Wounds International Vol 2 | Issue 1 | ©Wounds International 2011


ANTIMICROBIAL PEPTIDES The skin, as well as providing a physical barrier to prevent bacterial colonisation, also secretes small proteins called antimicrobial peptides (eg beta defensins), which are cationic proteins that kill bacteria by damaging their cell membranes. Moreover, additional antimicrobial peptides (eg cathelicidins) are released by cells in response to injury, such as wounding. These antimicrobial peptides act on the ‘frontline’ of the body to destroy invading bacteria.


MICROBIAL FLORA While the skin barrier is hostile to most bacteria, some species are able to survive, for example Staphylococcus epidermidis and the coryneform bacteria Propionibacterium acnes. Together these and other skin commensals (commensalism is a symbiotic relationship where the host is neither harmed nor helped) form the skin microflora, which prevent other potentially pathogenic microorganisms from achieving a foothold on the skin. Thus, it is the skin microflora that forms the body’s outermost environmental barrier.


These six aspects of skin biology combine


to form a barrier and protect our internal tissues from the potential harmful effects of the environment. Upon wounding, the normal skin barrier is breached and the dynamics of the host response to the environment are drastically changed to favour colonisation by potentially harmful microbes, thus rapid wound healing is essential to protect the host from the environment.


Figure 3 – The water barrier. Tight junctions


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