Reports of Biochemistry
and Molecular Biology
Mon, Oct 6, 2025
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Vol.14 No.1 Apr
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Department of Immunology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran & Cancer, petroleum, and environmental pollutants Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Abstract: (23 Views)
Background: Human second-degree burns can form blisters that allow burn wound microenvironment (WME) fluid to accumulate, which leads to inflammation. Different types of cells are present in burn WME, including macrophages; these innate immune cells are present in tumor microenvironments (TMEs) and burn WMEs. They adapt their phenotypes according to environmental stimuli, which vary from pro-inflammatory (M1) to anti-inflammatory (M2). It is evident that these microenvironments share some similarities in terms of macrophage plasticity; therefore, this study examines whether burn blister exudate (BBE) can enhance macrophage activity against CT-26 cancer cells by macrophage polarization.
Methods: Real-time PCR and ELISA were used to examine the effects of human BBE on untreated and M2 macrophages. As part of the immune response assessment, yeast phagocytosis was conducted. The impact of BBE-induced macrophages on CT-26 cancer cell survival and migration was assessed using MTT proliferation assay and scratch wound healing assay, respectively.
Results: According to the results, tumor necrosis factor-alpha, interferon regulatory factor 5, induced nitric oxide synthase, and CD86 were upregulated as M1-related markers and cytokines, and M2-associated cytokines and markers, transforming growth factor beta, IL-10, Fizz1, Arginase-1, and CD206, were downregulated in untreated and M2 macrophages treated with BBE. BBE also enhanced the phagocytic capacity of untreated and M2 macrophages. Furthermore, the incubated CT-26 cell line with conditioned medium of BBE treatment groups suppresses proliferation and impedes migration of cancer cells.
Conclusion: we found that BBE-treated macrophages possess an M1-like phenotype and inhibit the proliferation and motility of CT-26 cancer cells.
Methods: Real-time PCR and ELISA were used to examine the effects of human BBE on untreated and M2 macrophages. As part of the immune response assessment, yeast phagocytosis was conducted. The impact of BBE-induced macrophages on CT-26 cancer cell survival and migration was assessed using MTT proliferation assay and scratch wound healing assay, respectively.
Results: According to the results, tumor necrosis factor-alpha, interferon regulatory factor 5, induced nitric oxide synthase, and CD86 were upregulated as M1-related markers and cytokines, and M2-associated cytokines and markers, transforming growth factor beta, IL-10, Fizz1, Arginase-1, and CD206, were downregulated in untreated and M2 macrophages treated with BBE. BBE also enhanced the phagocytic capacity of untreated and M2 macrophages. Furthermore, the incubated CT-26 cell line with conditioned medium of BBE treatment groups suppresses proliferation and impedes migration of cancer cells.
Conclusion: we found that BBE-treated macrophages possess an M1-like phenotype and inhibit the proliferation and motility of CT-26 cancer cells.
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