Skin barrier and protection
Also known as: skin barrier, epidermal barrier, acid mantle, transepidermal water loss, TEWL, antimicrobial peptides, skin microbiome
The skin's protective barrier combines a physical layer (stratum corneum lipids and tight junctions), a chemical layer (acid pH, antimicrobial peptides, sebum), a microbial layer (commensals) and an immune layer (Langerhans cells, mast cells, T cells).
Overview
Physical barrier. The stratum corneum is organised like a brick wall: corneocytes (bricks) with cross-linked cornified envelopes and keratin–filaggrin cores are embedded in multilamellar lipid sheets (mortar) of ceramides, cholesterol and free fatty acids extruded from lamellar bodies. Tight junctions (claudin-1, occludin) in the stratum granulosum form a second seal. Filaggrin breakdown products form natural moisturising factor, keeping the corneum hydrated and flexible. Together these limit transepidermal water loss to ≈300–400 mL/day and exclude most water-soluble molecules; only small (<≈500 Da), lipophilic molecules penetrate well — the basis of transdermal drug patches (nicotine, fentanyl, oestradiol, glyceryl trinitrate).
Chemical barrier. The surface acid mantle (pH ≈4.5–5.5) from free fatty acids, lactic acid and urocanic acid inhibits pathogens and optimises lipid-processing enzymes. Keratinocytes and sweat contribute antimicrobial peptides — β-defensins, cathelicidin (LL-37), dermcidin, psoriasin — and sebum provides antimicrobial fatty acids.
Microbial and immune barriers. Commensals (Staphylococcus epidermidis, Cutibacterium acnes, Corynebacterium, Malassezia) compete with pathogens and tune immunity. Langerhans cells, dermal dendritic cells, macrophages, mast cells and resident memory T cells survey for invaders, and continuous desquamation sheds colonising microbes. Melanin caps protect DNA from UV, and the keratinised layers and dermal collagen resist mechanical trauma.
Function
- Prevents dehydration and loss of solutes
- Excludes microbes, allergens and toxins
- Absorbs UV radiation
- Resists friction, pressure and shear
Clinical significance
Atopic dermatitis and filaggrin
Loss-of-function filaggrin mutations (also causing ichthyosis vulgaris) weaken the barrier, increasing transepidermal water loss and allergen entry — the start of the "atopic march" to food allergy, asthma and rhinitis.
Barrier failure in burns and prematurity
Extensive burns cause massive evaporative fluid loss, protein loss, hypothermia and invasive infection (Pseudomonas, S. aureus). Very preterm infants lack a mature stratum corneum, so suffer high water loss and absorb topical agents (e.g. alcohol, iodine) dangerously.
Transdermal drug delivery
Drugs suited to patches are potent, small (<≈500 Da) and lipophilic; absorption is greater through thin, hydrated, inflamed or occluded skin and in areas like the scrotum and face.
Compiled from standard anatomy and physiology references — see the Integumentary System sources. For education only; not medical advice.