Background: Sulfur mustard (SM) is a blister-forming agent that has been used as a chemical weapon. Sulfur\r\nmustard can cause damage in various organs, especially the skin, respiratory system, and eyes. Generally, the\r\nmultiple complications of mustard gas result from its alkalizing potency; it reacts with cellular components like\r\nDNA, RNA, proteins, and lipid membranes.\r\nTGF-b is a multi-functional cytokine with multiple biological effects ranging from cell differentiation and growth\r\ninhibition to extracellular matrix stimulation, immunosuppression, and immunomodulation. TGF-b has 3 isoforms\r\n(TGF-b 1, 2, 3) and its signaling is mediated by its receptors: R1, R2 and intracellular Smads molecules.\r\nTGF-b has been shown to have anti-inflammatory effects. TGF-bs and their receptors also have an important role in\r\nmodulation of skin inflammation, proliferation of epidermal cells, and wound healing, and they have been\r\nimplicated in different types of skin inflammatory disorders.\r\nMethods: Seventeen exposed SM individuals (48.47 �± 9.3 years), 17 chronic dermatitis patients (46.52 �± 14.6 years),\r\nand 5 normal controls (44.00 �± 14.6 years) were enrolled in this study.\r\nEvaluation of TGF-bs and their receptors expressions was performed by semiquantitative RT-PCR. Only TGF1was\r\nanalyzed immunohistochemically.\r\nResults: Our results showed significant decreases in the expression percentages of TGF-b 1, 2 and R1, R2 in\r\nchemical victims in comparison with chronic dermatitis and normal subjects and significant decreases in the\r\nintensity of R1 and R2 expressions in chemical victims in comparison with chronic dermatitis and normal controls.\r\n(P value < 0.05)\r\nConclusions: TGF-bs and their receptors appear to have a noticeable role in chronic inflammatory skin lesions\r\ncaused by sulfur mustard.
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