Table 1.
Properties of sweat from patients with atopic dermatitis.
Fig 1.
The properties of sweat from patients with atopic dermatitis (AD) and healthy subjects (HS).
(a) Time required to obtain 5 ml of sweat (HS n = 10, AD n = 13). Analysis of: (b) pH (HS n = 10, AD n = 15); (c) protein concentration (HS n = 10, AD n = 17); (d) sodium concentration (HS n = 10, AD n = 14); and (e) other salt content (HS n = 9, AD n = 20). Concentration in sweat of anti-microbial peptides, including: (f) LL-37 (HS n = 6, AD n = 16); (g) dermcidin (HS n = 6, AD n = 17); and (h) β-defensin (HS n = 6, AD n = 17). F-test values represent individual variability within the sample.
Fig 2.
NMR spectra of sweat from patients with AD and HS.
(a) NMR spectra of the sweat from HS were characterized by intense lactate, pyruvate, and formate signals. A glucose peak was observed in sweat from AD. Glucose concentration was compared between (b) HS (n = 10) and AD (n = 21) and (c) between AD with eczema/exudative papules (ez/exu, n = 11), AD with lichenification/dermatitis (lich/der, (n = 10) and HS (n = 10). Key: (**p<0.01), unpaired t-test. (d) Correlation between disease severity (SCORAD) and properties of sweat. Statistical results are presented with Pearson’s correlation coefficients: pH, n = 16; protein concentration, n = 18; glucose concentration, n = 21; β-defensin, n = 18; and LL-37, n = 16.
Fig 3.
Impact of glucose on recovery of damaged stratum corneum in mice.
(a) Time course for measuring transepidermal water loss (TEWL) following tape stripping in the barrier disruption mouse model. (b) Changes in the TEWL value during the time course. Red triangles represent the glucose-treated group (n = 3), blue squares represent the vehicle-treated group (n = 3), and black circles represent the control group (n = 3). Error bars indicate mean ± SD. Key: (***) p<0.001 (glucose vs. control), (*) p<0.05 (glucose vs. water), Tukey’s multiple comparison. DDW, distilled deionized water; TS, tape stripping. These results are from one independent experiment; another is shown in S1 Fig.
Fig 4.
GLUT2 localization in skin from patients with AD.
The localization of GLUT2 (red) and smooth muscle actin (SMA; green) in healthy subjects (n = 3), patients with prurigo nodularis (n = 3), psoriasis (n = 3), AD with eczema/exudative papules (n = 8), or AD with dermatitis/lichenification (n = 3) as determined using immunofluorescence. Hoechst33322 was used to stain nuclei (blue). Representative data are presented. Scale bars are 100 μm.
Fig 5.
Expression of GLUT2 in sweat glands isolated from human skin.
(a) Hematoxylin and eosin staining of LMD-harvested sweat glands. (b) GLUT2 mRNA was significantly increased in sweat glands from patients with AD (n = 11) compared with those from HS (control; n = 8). (C) GLUT2 mRNA expression was compared between samples of AD with eczema/exudative papules (n = 6) and AD with dermatitis/lichenification (n = 5). Key: (***) p<0.001, unpaired t-test.
Fig 6.
Illustration of the sweat collection procedure.
Briefly, the whole back was wiped with tap water (STEP 1), and a drape with a 15×20 cm square hole was applied (STEP 2). Petrolatum was applied to the area in the hole (STEP 3). The bottom of the drape was folded up to create a pocket for fluid collection as subjects bathed in a sauna at 80°C (STEP 4). The sweat that pooled in the drape was collected with a syringe and filtered with a cartridge-type 0.22-μm filter.