Keratinocyte growth factor, interleukins (1 beta, 6, 8, 10, 12), and tumor necrosis factor alpha in culture medium of dermal fibroblast of burned patients

Abstract

. Conception, design, intellectual and scientific content of the study; analysis and interpretation of data; manuscript writing; critical revision. Abstract Purpose:To evaluate the level of cytokines and keratinocyte growth factor (KGF) or Fibroblast Growth Factor 7 (FGF-7) in the culture medium of cultured human dermal fibroblasts from patients with large burn in comparison to small burn. Methods:Fibroblasts of 10 patients (four large burns, four small burns and two controls) were initiated by the enzymatic method using collagenase. Cytokines and KGF in the supernatant of the culture medium was measured by, respectively, flow cytometry using Cytometric Bead Array Human Inflammation kit (CBA, BD Biosciences, USA) and the enzyme immunoassay method using the Quantikine ® Human KGF. The experiments were performed in triplicate. Results:The expression of IL-12 protein in patients with large burns showed a tendency to increase. IL-6, IL-10, and IL-1beta were observed no difference. For IL -8, TNF -alpha and KGF was observed a significant difference between the expression in large and small burned patient. Conclusion:That IL-8, TNF-alpha and KGF showed higher expression in cultured fibroblasts of large burned patients.

Early expression of IL-10, IL-12, ARG1, and NOS2 genes in peripheral blood mononuclear cells synergistically correlate with patient outcome after burn injury

“…Ingenuity Pathway Analysis identified multiple pathways related to IL-10 and inducible nitric oxide synthase (iNOS) signaling to have significant z scores 31–35 . This builds on our prior observations that an increase in IL-10 and a decrease in its pro-inflammatory counterpart, IL-12, are found after with burn injury 24,26,28,36–40 . Similarly, we have identified NOS2 (or iNOS) to correlate with the response to burn injury, whereby ARG1, a key regulator of inflammation-associated immunosuppression, 1,41,42 negatively regulates NOS2 43 .…”

“…[31][32][33][34][35] This builds on our prior observations that an increase in IL-10 and a decrease in its proinflammatory counterpart, IL-12, are found after with burn injury. 24,26,28,[36][37][38][39][40] Similarly, we have identified NOS2 (or iNOS) Figure 1. Burn injury induces altered gene expression profiles and resultant pathway scores.…”

Anti-inflammatory effects of low-level laser in burn wound models in rats

“…Thermal burn injuries to the skin may respond with inflammation, cellular protection mechanisms, immune suppression, hypermetabolic dysfunction or organs [6,7]. Pain may be due to skin inflammation, along with the appearance of exudate and cytokine production such as tumor necrosis factor (TNF)-α and interleukins (IL) such as IL-6, IL-8 and IL-10 [8,9]. In particular, TNF-α and IL-6 are known to have a complex anti-inflammatory role in burn wound pathogenesis by commencing inflammatory responses [10,11].…”