High in situ mRNA levels of IL-22, TFG-ß, and ARG-1 in keloid scars.

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-ß, 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-ß, 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.

In Situ Cytokine Expression and Morphometric Evaluation of Total Collagen and Collagens Type I and Type III in Keloid Scars.

Keloids are characterized by excessive collagen deposition and growth beyond the edges of the initial injury, and cytokines may be related to their formation. The objective of this study was to evaluate the collagen fibers, analyze in situ expression of cytokines in keloid lesions, and compare to the control group. Results showed that there was a predominance of women and nonwhite and direct black ancestry. Keloid showed a significant increase in total and type III collagen. Significantly, the expression of mRNA for TGF-ß in keloid was increased, the expressions of IFN-γ, IFN-γR1, and IL-10 were lower, and IFN-γR1 and TNF-α had no statistical difference. Correlations between collagen type III and TGF-ß mRNA expression were positive and significant, IFN-γ, IFN-γR1, and IL-10 were negative and significant, and TNF-α showed no statistical difference. We conclude that there was a significant increase of total collagen in keloid and predominance of collagen type III compared to the controls, showing keloid as an immature lesion. There is a significant increase in TGF-ß mRNA in keloid lesions, and a significant decrease in IFN-γ and IL-10, suggesting that these cytokines are related to keloid lesions.