Physiologic Lipids for Barrier Repair in Dermatology

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Chapter 10 Physiologic Lipids for Barrier Repair in Dermatology


Although the stratum corneum (SC) serves many defensive functions (Table 10.1), none is as important as its ability to prevent excess loss of fluids and electrolytes, i.e. the permeability barrier. Permeability barrier function is mediated by the organization of the extracellular lipids of the SC into a series of parallel lamellar membranes, which mediate not only permeability barrier function, but also additional, key protective functions of the epidermis (Fig. 10.1). The functions of the SC can be further localized to either the cellular (corneocyte) compartment or extracellular matrix (Table 10.1).

Table 10.1 Protective functions of mammalian stratum corneum

Function Localization
Permeability barrier* Extracellular
Initiation of inflammation (cytokine activation)* Corneocyte (and granular cell)
Cohesion (Integrity) → Desquamation* Extracellular
Antimicrobial barrier (innate immunity)* Extracellular
Mechanical (impact and shear resistance) Corneocyte
Toxic chemical/antigen exclusion Extracellular
Selective absorption Extracellular
Hydration Corneocyte
UV barrier Corneocyte
Psychosensory interface Unknown
Thermal barrier Unknown

* Regulated by SC pH.


The skin barrier is assaulted frequently in daily life by hot water, detergents, solvents, mechanical trauma, and occupation-related chemicals. If these insults are frequently repeatedly and/or insufficiently repaired, they threaten the organism with desiccation due to accelerated transepidermal water loss (TEWL). To avoid this outcome, the underlying epidermis mounts a coordinated metabolic response, ranging from increased lipid synthesis to accelerated lipid secretion, aimed at rapidly restoring normal function. This response is elicited by any type of barrier insult (e.g. organic solvents, detergents, tape stripping) that depletes the SC of its complement of lipids. Although the total time required for barrier recovery varies according to age, there is an initial, rapid recovery phase that leads to 50–60% recovery in young humans in about 12 hours, with full recovery requiring about 3 days (Fig. 10.2). But in aged humans (> 75 years), complete recovery from comparable insults is prolonged to about 1 week. Restoration of barrier function is accompanied by reaccumulation of lipids, visible with either oil red O staining or Nile red fluorescence, and by the reappearance of membrane structures within the SC interstices, as early as 2 hours after acute disruption. Because artificial restoration of the barrier with vapor-impermeable membranes inhibits barrier recovery, as well as all of the metabolic processes linked to it, the entire metabolic response represents a response that is aimed specifically at restoring normal permeability barrier homeostasis.