da Cunha Colombo Tiveron Luciana Rodrigues, da Silva Isabela Rios, da Silva Marcos Vinicius, Peixoto Alberto Borges, Rodrigues Denise Bertulucci Rocha, Rodrigues Virmondes
Federal University of Triângulo Mineiro (UFTM) ICBN and CEFORES, Uberaba, MG, Brazil.
Laboratory of Biopathology and Molecular Biology, University of Uberaba (UNIUBE), Uberaba, MG, Brazil.
Immunobiology. 2018 Dec;223(12):812-817. doi: 10.1016/j.imbio.2018.08.010. Epub 2018 Aug 20.
Keloid scars are currently considered a chronic inflammatory process and no longer a benign skin tumor. Keloids are defined as highly inflamed, hyperproliferative pathological scars. Growth factors and cytokines have important functions in the keloid inflammatory etiopathogenesis. The aim of this study was to analyze the in situ expression of cytokines and growth factors in keloid scars in comparison with that in normal scars. Among them, we specifically assessed TGF-β, FGF, IL-33, IL-22, ARG-1, ARG-2, iNOS, VIP, VIP-R1, TAC, and TAC-R1. A total of 98 biopsies were evaluated, including of 53 keloid and 45 normal scars. The age of patients with keloids ranged from 11 to 73 years, with a mean age of 28 years and predominance of the female gender (58.5% of the total patients). Around 64.15% of the patients belonged to the black ethnic group. Evaluated keloids were most commonly located in the earlobe because of ear piercing, representing 73.6% of the cases. We found significantly greater expression of TGF-β, IL-22, and ARG-1 in keloids when compared with that in normal scars. As for IL-33, ARG-2, and VIP-R1, despite the higher number of mRNA copies found in keloids, this difference was not significant. Furthermore, FGF, iNOS, VIP, TAC, and TAC-R1 mRNA levels were not detectable, and therefore these results were inconclusive in this study. Considering these results, understanding the cellular and molecular mechanisms that control the inflammatory response during cutaneous healing may promote the development of strategies to improve the treatment of patients with keloids.
瘢痕疙瘩目前被认为是一种慢性炎症过程,而非良性皮肤肿瘤。瘢痕疙瘩被定义为高度炎症性、过度增殖性的病理性瘢痕。生长因子和细胞因子在瘢痕疙瘩的炎症发病机制中具有重要作用。本研究的目的是分析瘢痕疙瘩中细胞因子和生长因子的原位表达,并与正常瘢痕进行比较。其中,我们特别评估了转化生长因子-β(TGF-β)、成纤维细胞生长因子(FGF)、白细胞介素-33(IL-33)、白细胞介素-22(IL-22)、精氨酸酶-1(ARG-1)、精氨酸酶-2(ARG-2)、诱导型一氧化氮合酶(iNOS)、血管活性肠肽(VIP)、血管活性肠肽受体1(VIP-R1)、促甲状腺素(TAC)和促甲状腺素受体1(TAC-R1)。共评估了98份活检样本,包括53例瘢痕疙瘩和45例正常瘢痕。瘢痕疙瘩患者的年龄范围为11至73岁,平均年龄为28岁,女性占优势(占总患者的58.5%)。约64.15%的患者属于黑人种族。评估的瘢痕疙瘩最常见于因穿耳洞而导致的耳垂,占病例的73.6%。我们发现,与正常瘢痕相比,瘢痕疙瘩中TGF-β、IL-22和ARG-1的表达明显更高。至于IL-33、ARG-2和VIP-R1,尽管在瘢痕疙瘩中发现的mRNA拷贝数较多,但这种差异并不显著。此外,未检测到FGF、iNOS、VIP、TAC和TAC-R1的mRNA水平,因此这些结果在本研究中尚无定论。考虑到这些结果,了解控制皮肤愈合过程中炎症反应的细胞和分子机制可能会促进改善瘢痕疙瘩患者治疗策略的发展。