Researches on MicroRNAs Expression Profiles in Lesions of Atopic Dermatitis Patients with Different Syndromes

OBJECTIVE To explore the relationship between expression profiles of microRNAs and chemokines and Chinese medicine syndromes in the skin lesions of patients with atopic dermatitis. METHODS 79 patients of AD were divided into three groups(group of internal damp-heat accumulation， group of excessive dampness due to spleen deficiency and group of blood deficiency and wind-dryness) according to syndrome differentiation. The qPCR and immunohistochemistry techniques were used to detect the expression characteristics of five microRNAs and three chemokines related to skin inflammations in AD. Immunoregulation of these differential expressions were statistically analyzed. RESULTS Increased expression levels of miR21 and decreased expression levels of miR125b were seen in the group of internal damp-heat accumulation， which were significantly different from the normal control group and the group of blood deficiency and wind-dryness(P<0.01). At the same time the higher expression of TARC/CCL17 was noticed and the positive molecules were seen located in the basal layer of the epidermis and dermis. The expression of miR-155 was significantly higher than the other two groups and the normal control group in the group(P<0.01). The expression of miR203 decreased， but no statistically significant difference were noticed when compared to the other groups(P>0.05). The highest expression of CTACK/CCL27 molecules were seen scattered in the epidermis and dermis. In the group of blood deficiency and wind-dryness， miR-146 expression has been raised， with significant statistical difference from the other groups(P<0.01). RANTES/CCL5 expression increased， higher than the group of internal damp-heat accumulation（P<0.01）. The same change was seen for TARC/CCL17 expression. CONCLUSION The microRNA expression profiles differentially expressed in AD patients with different syndromes， leading to different inflammatory tissue damages. These findings reveal the pathogenesis molecular mechanisms of AD.