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. 2019 Jun 3;11(5):677–690. doi: 10.4168/aair.2019.11.5.677

Fig. 2. ALCAM attenuates skin barrier disruption induced by epicutaneous OVA sensitization. (A) Time course of clinical score and (B) TEWL. (C) Electron micrographs of osmium tetroxide-postfixed skins show LBs in SG (×50,000, Scale bar = 0.5 μm; Insert C). (Left) Normal shaped LBs are present in sham mouse epidermis. (Middle) WT/OVA mouse epidermis shows severely abnormal LBs, (Right) Whereas LBs in ALCAM−/− mice display less abnormality (×120,000, Scale bar = 0.2 μm). (D) Bar graph represents the number of LBs in SG. (E) The mRNA expression of skin barrier genes (filaggrin, loricrin and involucrin).

Fig. 2

The data represent mean ± standard error of the mean.

ALCAM, activated leukocyte cell adhesion molecule; TEWL, transepidermal water loss; OVA, ovalbumin; PBS, phosphate-buffered saline; NS, not significant; WT, wild-type; LB, lamellar body; mRNA, messenger RNA; SG, stratum granulosum.

*P < 0.05 (WT/PBS vs. WT/OVA); P < 0.05 (ALCAM−/−/PBS vs. ALCAM−/−/OVA); P < 0.05 (WT/OVA vs. ALCAM−/−/OVA); §P < 0.05; P < 0.01; P < 0.001 (n = 5–7 mice/group).