Azza G A Farag1, Mostafa A Hammam1, Hesham N Khaled1, ShimaE Soliman2, Nermin Reda Tayel3, Amira A El-Shamendy4, Wafaa A Shehata1. 1. Department of Dermatology, Andrology and STDs, Faculty of Medicine, Menoufia University, Shebin ElKom, Egypt. 2. Department of Biochemistry, Faculty of Medicine, Menoufia University, Shebin ElKom, Egypt. 3. Department of Molecular Diagnostics and Therapeutics, Genetic Engineering Biotechnology Research Institute, Sadat City, Egypt. 4. Ministry of Heath, Shebin Alkom Teaching Hospital, Al- Menoufia, Egypt.
Abstract
BACKGROUND/ OBJECTIVES: Atopic dermatitis (AD) is an inflammatory chronic skin disorder. The etiology of AD is not fully understood. Therefore, we aimed by this study to shed light on the potential role of resistin in an etiopathogenesis of AD through investigation of resistin rs3745367 single nucleotide polymorphism (SNP) and resistin serum levels, and their relation to leukocytic count in a sample of Egyptian patients having atopic dermatitis. METHODS: This case-control study included 45 patients having AD and 40 controls. SCORAD index was assessed to evaluate the severity of AD. CBC, ELISA, and PCR-RFLP were performed to detect leukocytic count, resistin serum level, and resistin rs3745367 SNP, respectively. RESULTS: Atopic dermatitis patients had significant low serum resistin concentrations (P = .036) and a significantly high frequency of leukocytosis (P = .003). Low resistin serum levels were significantly related to AD disease severity (P < .001) and the presence of leukocytosis (P < .001). Resistin rs3745367 GG genotype (P = .030), as well as its G allele (P = .019), was expressively associated with AD development, and both increased the risk of AD by 3- and 2-fold, respectively. Resistin rs3745367 GG genotype was significantly linked to low resistin serum levels (P < .001), AD-positive family history (P = .015), and the presence of leukocytosis (P < .001). CONCLUSIONS: Resistin rs3745367 gene polymorphism may contribute to the development of AD. Resistin may have an immune-modulating active character in the AD etiopathogenesis that could be mediated through its anti-inflammatory effect. From this piece of work, we may suggest resistin as a new therapy to mitigate the pro-inflammatory environment found in AD.
BACKGROUND/ OBJECTIVES: Atopic dermatitis (AD) is an inflammatory chronic skin disorder. The etiology of AD is not fully understood. Therefore, we aimed by this study to shed light on the potential role of resistin in an etiopathogenesis of AD through investigation of resistin rs3745367 single nucleotide polymorphism (SNP) and resistin serum levels, and their relation to leukocytic count in a sample of Egyptian patients having atopic dermatitis. METHODS: This case-control study included 45 patients having AD and 40 controls. SCORAD index was assessed to evaluate the severity of AD. CBC, ELISA, and PCR-RFLP were performed to detect leukocytic count, resistin serum level, and resistin rs3745367 SNP, respectively. RESULTS: Atopic dermatitis patients had significant low serum resistin concentrations (P = .036) and a significantly high frequency of leukocytosis (P = .003). Low resistin serum levels were significantly related to AD disease severity (P < .001) and the presence of leukocytosis (P < .001). Resistin rs3745367 GG genotype (P = .030), as well as its G allele (P = .019), was expressively associated with AD development, and both increased the risk of AD by 3- and 2-fold, respectively. Resistin rs3745367 GG genotype was significantly linked to low resistin serum levels (P < .001), AD-positive family history (P = .015), and the presence of leukocytosis (P < .001). CONCLUSIONS: Resistin rs3745367 gene polymorphism may contribute to the development of AD. Resistin may have an immune-modulating active character in the AD etiopathogenesis that could be mediated through its anti-inflammatory effect. From this piece of work, we may suggest resistin as a new therapy to mitigate the pro-inflammatory environment found in AD.
Authors: Carlos Jiménez-Cortegana; Germán Ortiz-García; Amalia Serrano; David Moreno-Ramírez; Víctor Sánchez-Margalet Journal: Biomolecules Date: 2021-11-05