The mRNA levels of COL1A1, COL2A1, COL3A1 and COL4A1 in non-lesional and lesional skin of atopic dermatitis patients.

Atopic dermatitis (AD) is a complex, multifactorial inflammatory disease. The multifaceted aetiology and pathophysiology consist of different elements, including genetic and immunological disorders, skin barrier defects, microbiome dysbiosis and environmental interactions. To date, little has been known about the genes involved in the relationship between extracellular matrix (ECM) expression and the pathogenesis of atopic dermatitis. The aim of our study was to examine the mRNA transcript levels of genes encoding collagen type I, II, III and IV in the skin of atopic dermatitis patients vs. controls and to search for associations with subjective clinical symptoms and disease severity. A total of 18 subjects participated in the study. Nine biopsies were taken from lesions, nine from non-lesional AD skin and nine from healthy volunteers. The mRNA levels of COL1A1, COL2A1, COL3A1 and COL4A1 were determined using real-time RT-PCR. AD severity was evaluated by calculating the SCORAD score and measuring the pruritus intensity using the Visual Analogue Scale (VAS). A significant increase in the mRNA levels of COL3A1 in the study group compared to the control group was associated with an increase in the intensity of clinically reported symptoms as assessed by the SCORAD and the itching scale VAS (p = 0.0293). In addition, there was a statistically significant difference in the mRNA levels of the COL3A1 gene and the mRNA levels of the COL4A1 gene between subjects in the lesional and non-lesional skin of the study group. The transcript level of mRNA COL3A1 was statistically higher in lesional skin than in non-lesional skin among subjects with AD than in healthy volunteers. Conversely, mRNA COL4A1 expression was significantly higher in non-lesional skin than in lesional skin among AD subjects; however, there was no statistical difference between AD subjects and healthy volunteers. Our results suggest a role for collagen mRNA levels in AD pathogenesis. Further studies are needed to assess its role as a new potential biomarker, as a predictive element for assessing the intensity of AD or as a new target for AD therapy in the era of personalized medicine. The question to be answered is the importance of remodelling processes in AD.