Skip to main content
Top
Published in: Inflammation 4/2019

01-08-2019 | ORIGINAL ARTICLE

Severe Burn Injury Progression and Phasic Changes of Gene Expression in Mouse Model

Authors: Dan Wu, Ming Zhou, Liang Li, Xiangfeng Leng, Zheng Zhang, Ning Wang, Yanwei Sun

Published in: Inflammation | Issue 4/2019

Login to get access

Abstract

Patients with severe burns are susceptible to infectious complications including burn-site infections and sepsis. The purpose of this study was to explore the pathologic development of burn injury in a mouse model and to screen genes dysregulated at different time points on the basis of gene expression microarrays. Differential expression analysis identified a total 223 genes that related to only time progression independent of burn injury and 214 genes with aberrant expression due to burn injury. Weighted gene co-expression network analysis (WGCNA) of the 214 genes obtained seven gene modules which named as red, blue, turquoise, green, brown, yellow, and gray module, and the blue module was found to be significantly associated with severe burn injury progression, and in which several genes were previously reported being associated with inflammation and immune response, such as interleukin IL-6, IL-8, and IL-1b. Functional enrichment analysis indicated significant enrichment of biological processes that related to metabolism and catabolism, and pathways of proteasome, notch signaling and cell cycle. This result supports a phase progression of severe burn with gene expression changes and interpretation of biological processes in mouse.
Appendix
Available only for authorised users
Literature
2.
go back to reference Lloyd, E.C., B.C. Rodgers, M. Michener, and M.S. Williams. 2012. Outpatient burns: prevention and care. American Family Physician 85 (1): 25–32.PubMed Lloyd, E.C., B.C. Rodgers, M. Michener, and M.S. Williams. 2012. Outpatient burns: prevention and care. American Family Physician 85 (1): 25–32.PubMed
8.
14.
go back to reference Barber, R.C., L.Y. Chang, B.D. Arnoldo, G.F. Purdue, J.L. Hunt, J.W. Horton, et al. 2006. Innate immunity SNPs are associated with risk for severe sepsis after burn injury. Clinical Medicine & Research 4 (4): 250–255.CrossRef Barber, R.C., L.Y. Chang, B.D. Arnoldo, G.F. Purdue, J.L. Hunt, J.W. Horton, et al. 2006. Innate immunity SNPs are associated with risk for severe sepsis after burn injury. Clinical Medicine & Research 4 (4): 250–255.CrossRef
19.
26.
go back to reference Kupper, T.S., E.A. Deitch, C.C. Baker, and W.C. Wong. 1986. The human burn wound as a primary source of interleukin-1 activity. Surgery. 100 (2): 409–415.PubMed Kupper, T.S., E.A. Deitch, C.C. Baker, and W.C. Wong. 1986. The human burn wound as a primary source of interleukin-1 activity. Surgery. 100 (2): 409–415.PubMed
27.
go back to reference Nickoloff, B.J., G.D. Karabin, J.N. Barker, C.E. Griffiths, V. Sarma, R.S. Mitra, J.T. Elder, S.L. Kunkel, and V.M. Dixit. 1991. Cellular localization of interleukin-8 and its inducer, tumor necrosis factor-alpha in psoriasis. The American Journal of Pathology 138 (1): 129–140.PubMedPubMedCentral Nickoloff, B.J., G.D. Karabin, J.N. Barker, C.E. Griffiths, V. Sarma, R.S. Mitra, J.T. Elder, S.L. Kunkel, and V.M. Dixit. 1991. Cellular localization of interleukin-8 and its inducer, tumor necrosis factor-alpha in psoriasis. The American Journal of Pathology 138 (1): 129–140.PubMedPubMedCentral
28.
go back to reference Sehgal, P.B. 1990. Interleukin-6: molecular pathophysiology. The Journal of Investigative Dermatology 94 (6 Suppl): 2S–6S.CrossRef Sehgal, P.B. 1990. Interleukin-6: molecular pathophysiology. The Journal of Investigative Dermatology 94 (6 Suppl): 2S–6S.CrossRef
29.
go back to reference Gosain, A., and R.L. Gamelli. 2005. A primer in cytokines. The Journal of Burn Care & Rehabilitation 26 (1): 7–12.CrossRef Gosain, A., and R.L. Gamelli. 2005. A primer in cytokines. The Journal of Burn Care & Rehabilitation 26 (1): 7–12.CrossRef
30.
go back to reference Hultman, C.S., L.M. Napolitano, B.A. Cairns, L.A. Brady, C. Campbell, S. deSerres, et al. 1995. The relationship between interferon-gamma and keratinocyte alloantigen expression after burn injury. Annals of Surgery 222 (3): 384–389 discussion 92-3.CrossRef Hultman, C.S., L.M. Napolitano, B.A. Cairns, L.A. Brady, C. Campbell, S. deSerres, et al. 1995. The relationship between interferon-gamma and keratinocyte alloantigen expression after burn injury. Annals of Surgery 222 (3): 384–389 discussion 92-3.CrossRef
31.
go back to reference Kock, A., T. Schwarz, R. Kirnbauer, A. Urbanski, P. Perry, J.C. Ansel, et al. 1990. Human keratinocytes are a source for tumor necrosis factor alpha: evidence for synthesis and release upon stimulation with endotoxin or ultraviolet light. The Journal of Experimental Medicine 172 (6): 1609–1614.CrossRef Kock, A., T. Schwarz, R. Kirnbauer, A. Urbanski, P. Perry, J.C. Ansel, et al. 1990. Human keratinocytes are a source for tumor necrosis factor alpha: evidence for synthesis and release upon stimulation with endotoxin or ultraviolet light. The Journal of Experimental Medicine 172 (6): 1609–1614.CrossRef
37.
go back to reference Moraru, M., E. Cisneros, N. Gómez-Lozano, R. de Pablo, F. Portero, M. Cañizares, M. Vaquero, G. Roustán, I. Millán, M. López-Botet, and C. Vilches. 2012. Host genetic factors in susceptibility to herpes simplex type 1 virus infection: contribution of polymorphic genes at the interface of innate and adaptive immunity. The Journal of Immunology 4: 1103434. https://doi.org/10.4049/jimmunol.1103434.CrossRef Moraru, M., E. Cisneros, N. Gómez-Lozano, R. de Pablo, F. Portero, M. Cañizares, M. Vaquero, G. Roustán, I. Millán, M. López-Botet, and C. Vilches. 2012. Host genetic factors in susceptibility to herpes simplex type 1 virus infection: contribution of polymorphic genes at the interface of innate and adaptive immunity. The Journal of Immunology 4: 1103434. https://​doi.​org/​10.​4049/​jimmunol.​1103434.CrossRef
38.
go back to reference Mbarek, H., Y. Milaneschi, J.J. Hottenga, L. Ligthart, E.J. de Geus, E.A. Ehli, G. Willemsen, G.E. Davies, J.H. Smit, D.I. Boomsma, and B.W. Penninx. 2017. Genome-wide significance for PCLO as a gene for major depressive disorder. Twin Research and Human Genetics 20 (4): 267–270. https://doi.org/10.1017/thg.2017.30.CrossRefPubMed Mbarek, H., Y. Milaneschi, J.J. Hottenga, L. Ligthart, E.J. de Geus, E.A. Ehli, G. Willemsen, G.E. Davies, J.H. Smit, D.I. Boomsma, and B.W. Penninx. 2017. Genome-wide significance for PCLO as a gene for major depressive disorder. Twin Research and Human Genetics 20 (4): 267–270. https://​doi.​org/​10.​1017/​thg.​2017.​30.CrossRefPubMed
39.
go back to reference Zhan, H., J. Jiang, Q. Sun, A. Ke, J. Hu, Z. Hu, K. Zhu, C. Luo, N. Ren, J. Fan, and J. Zhou. 2017. Whole-exome sequencing-based mutational profiling of hepatitis B virus-related early-stage hepatocellular carcinoma. Gastroenterology Research and Practice. https://doi.org/10.1155/2017/2029315. Zhan, H., J. Jiang, Q. Sun, A. Ke, J. Hu, Z. Hu, K. Zhu, C. Luo, N. Ren, J. Fan, and J. Zhou. 2017. Whole-exome sequencing-based mutational profiling of hepatitis B virus-related early-stage hepatocellular carcinoma. Gastroenterology Research and Practice. https://​doi.​org/​10.​1155/​2017/​2029315.
43.
go back to reference Alexander, J.W. 1990. Mechanism of immunologic suppression in burn injury. The Journal of Trauma 30 (12 Suppl): S70–S75.CrossRef Alexander, J.W. 1990. Mechanism of immunologic suppression in burn injury. The Journal of Trauma 30 (12 Suppl): S70–S75.CrossRef
44.
go back to reference Faunce, D.E., M.S. Gregory, and E.J. Kovacs. 1997. Effects of acute ethanol exposure on cellular immune responses in a murine model of thermal injury. Journal of Leukocyte Biology 62 (6): 733–740.CrossRef Faunce, D.E., M.S. Gregory, and E.J. Kovacs. 1997. Effects of acute ethanol exposure on cellular immune responses in a murine model of thermal injury. Journal of Leukocyte Biology 62 (6): 733–740.CrossRef
45.
go back to reference Gamelli, R.L., L.K. He, and H. Liu. 1994. Marrow granulocyte-macrophage progenitor cell response to burn injury as modified by endotoxin and indomethacin. The Journal of Trauma 37 (3): 339–346.CrossRef Gamelli, R.L., L.K. He, and H. Liu. 1994. Marrow granulocyte-macrophage progenitor cell response to burn injury as modified by endotoxin and indomethacin. The Journal of Trauma 37 (3): 339–346.CrossRef
46.
go back to reference Hansbrough, J.F., R. Zapata-Sirvent, V. Peterson, X. Wang, E. Bender, H. Claman, et al. 1984. Characterization of the immunosuppressive effect of burned tissue in an animal model. The Journal of Surgical Research 37 (5): 383–393.CrossRef Hansbrough, J.F., R. Zapata-Sirvent, V. Peterson, X. Wang, E. Bender, H. Claman, et al. 1984. Characterization of the immunosuppressive effect of burned tissue in an animal model. The Journal of Surgical Research 37 (5): 383–393.CrossRef
50.
go back to reference Çakir, B., and B.C. Yeğen. 2004. Systemic responses to burn injury. Turkish Journal of Medical Sciences 34 (4): 215–226. Çakir, B., and B.C. Yeğen. 2004. Systemic responses to burn injury. Turkish Journal of Medical Sciences 34 (4): 215–226.
59.
go back to reference Bombaro, K.M., L.H. Engrav, G.J. Carrougher, S.A. Wiechman, L. Faucher, B.A. Costa, D.M. Heimbach, F.P. Rivara, and S. Honari. 2003. What is the prevalence of hypertrophic scarring following burns? Burns: Journal of the International Society for Burn Injuries 29 (4): 299–302.CrossRef Bombaro, K.M., L.H. Engrav, G.J. Carrougher, S.A. Wiechman, L. Faucher, B.A. Costa, D.M. Heimbach, F.P. Rivara, and S. Honari. 2003. What is the prevalence of hypertrophic scarring following burns? Burns: Journal of the International Society for Burn Injuries 29 (4): 299–302.CrossRef
62.
go back to reference Valenti, L.M., J. Mathieu, Y. Chancerelle, M. De Sousa, M. Levacher, A.T. Dinh-Xuan, and I. Florentin. 2005. High levels of endogenous nitric oxide produced after burn injury in rats arrest activated T lymphocytes in the first G1 phase of the cell cycle and then induce their apoptosis. Experimental Cell Research 306 (1): 150–167. https://doi.org/10.1016/j.yexcr.2005.02.008.CrossRefPubMed Valenti, L.M., J. Mathieu, Y. Chancerelle, M. De Sousa, M. Levacher, A.T. Dinh-Xuan, and I. Florentin. 2005. High levels of endogenous nitric oxide produced after burn injury in rats arrest activated T lymphocytes in the first G1 phase of the cell cycle and then induce their apoptosis. Experimental Cell Research 306 (1): 150–167. https://​doi.​org/​10.​1016/​j.​yexcr.​2005.​02.​008.CrossRefPubMed
Metadata
Title
Severe Burn Injury Progression and Phasic Changes of Gene Expression in Mouse Model
Authors
Dan Wu
Ming Zhou
Liang Li
Xiangfeng Leng
Zheng Zhang
Ning Wang
Yanwei Sun
Publication date
01-08-2019
Publisher
Springer US
Published in
Inflammation / Issue 4/2019
Print ISSN: 0360-3997
Electronic ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-019-00984-5

Other articles of this Issue 4/2019

Inflammation 4/2019 Go to the issue