Man Mao-Qiang

Cutaneous Permeability Barrier Repair following Various Types of Insults: Kinetics and Effects of Occlusion

Previous studies have shown that acute disruption of the cutaneous permeability barrier by acetone results in an initial rapid phase of repair followed by a later, slower phase. In the present study, we demonstrate that manipulations which disrupt the barrier by other mechanisms, such as tape stripping or detergent treatment, have a similar pattern of barrier repair. In all three models, the return of lipid to the stratum corneum parallels the normalization of barrier function, and occlusion immediately after disrupting the barrier blocks both the return of lipid and the normalization of function. Moreover, occlusion beginning 6-8 h following barrier disruption blocks the late, slower phase of repair, indicating that the late phase can be inhibited independently of the initial phase. Lastly, both severe and relatively minor perturbations of the barrier elicit a repair response with a similar kinetic pattern. In summary, the present study demonstrates that barrier repair responses are similar regardless of the etiology or extent of barrier disruption.

Role of Exogenous Oxygen in Cutaneous Barrier Repair

Occlusion of the skin with a water-vapor-impermeable membrane following disruption of the permeability barrier prevents the epidermal changes which lead to the restoration of barrier function, suggesting that water transit could be an important regulatory signal for barrier repair. However, occlusion with a water-vapor-impermeable membrane also prevents the movement of gases, which could also potentially influence permeability barrier homeostasis. Since O2 is known to have an effect on epidermal cell function, we have determined the effect of gases containing different levels of O2 on barrier repair 6 h following topical treatment of hairless mice with acetone. The disrupted barrier of air-exposed animals (O2 approximately 20%) recovered by 50.8 +/- 3.4% (mean +/- SEM) after 6 h. Under flowing air (O2 approximately 20%), O2/CO2 95/5% and argon (O2 = 0%) the barrier recovered by 43.9 +/- 28, 36.2 +/- 8.5 and 39.2 +/- 4.6%, respectively. These values were not statistically different from each other. The slightly lower levels of recovery at 6 h with the flowing gases in comparison to exposure to static air probably can be attributed to a slight cooling of the skin caused by the flowing gases. These results suggest that exogenous O2 is neither required for barrier repair nor a signal for barrier repair.