Pathophysiological role of chemokine MIG/CXCL9 in the development of atopic dermatitis

Abstract

Background. In patients with atopic dermatitis, the persistence of microorganisms on the skin surface is high, which can enhance the expression of MIG/CXCL9, exacerbating inflammation and activating keratinocyte apoptosis, however, the dynamics of this chemokine in atopic dermatitis has not been studied.The aim. To study the concentration of chemokine MIG/CXCL9 in the dynamics of atopic dermatitis and determine its role in the pathogenesis of dermatosis.Materials and methods. The study included 80 patients aged 13 to 44 years with limited and widespread atopic dermatitis and 30 practically healthy volunteers. The therapy of patients, the collection of biological material were carried out in the Regional Dermatovenerologic Dispensary in Chita, laboratory tests were performed at the Chita State Medical Academy in the period from 2018 to 2020. The MIG/CXCL9 level was studied during exacerbation and remission of the disease in blood serum and skin exudate by flow cytofluorimetry using LEGENDplex Human Proinflammatory Chemokine Panel (BioLegend, USA). In healthy volunteers, skin exudate sampling was carried out by the “skin window” method. For statistical processing, the Microsoft Excel (Microsoft Corp., USA) application software package and SPSS Statistics 25.0 (IBM Corp., USA) were used.Results. The concentration of chemokine MIG/CXCL9 in the skin exudate is greater than in the blood serum. With a limited form of the disease in adolescents, the level of MIG/CXCL9 in the skin exudate is 8.1 times higher than the control values, with a common form – 9.3 times. In adults with advanced atopic dermatitis, the concentration of chemokine IL/CXCL9 in the skin exudate is 20.8 times higher than the values of the control group.Conclusion. In atopic dermatitis, the level of chemokine MIG/CXCL9 is higher in the cutaneous pathological process. In the pathogenesis of the disease, MIG/ CXCL9 inhibits collagen synthesis and promotes apoptosis of keratinocytes, followed by the formation of hyperreactivity of the skin, its dryness and peeling.