Early Transcriptomic Response to Burn injury: Severe Burns are Associated with Immune Pathway Shutdown. Early Transcriptomic Response to Burn Injury: Severe Burns Are Associated With Immune Pathway Shutdown.

MedStar author(s):
Citation: Journal of Burn Care & Research. 43(2):306-314, 2022 03 23.PMID: 34791339Institution: MedStar Health Research Institute | MedStar Washington Hospital CenterDepartment: Burn Research Fellowship | Firefighters' Burn and Surgical Research Laboratory | Surgery/Burn ServicesForm of publication: Journal ArticleMedline article type(s): Journal ArticleSubject headings: *Burns | *Transcriptome | Adult | Body Surface Area | Burns/ge [Genetics] | Female | Gene Expression Regulation | Humans | Male | Microarray Analysis | Middle Aged | Retrospective StudiesYear: 2022Local holdings: Available online through MWHC library: 2006 - present, Available in print through MWHC library: 2006 - presentISSN:
  • 1559-047X
Name of journal: Journal of burn care & research : official publication of the American Burn AssociationAbstract: Burn injury induces a systemic hyperinflammatory response with detrimental side effects. Studies have described the biochemical changes induced by severe burns, but the transcriptome response is not well characterized. The goal of this work is to characterize the blood transcriptome after burn injury. Burn patients presenting to a regional center between 2012-2017 were prospectively enrolled. Blood was collected on admission and at predetermined time points (hours 2, 4, 8, 12, 24). RNA was isolated and transcript levels were measured with a gene expression microarray. To identify differentially regulated genes (FDR<=0.1) by burn injury severity, patients were grouped by total body surface area (TBSA) above or below 20% and statistically enriched pathways were identified. Sixty-eight patients were analyzed, most patients were male with a median age of 41 (IQR, 30.5-58.5) years, and TBSA of 20% (11-34%). Thirty-five patients had %TBSA injury >=20%, and this group experienced greater mortality (26% vs. 3%, p=0.008). Comparative analysis of genes from patients with </>=20% TBSA revealed 1505, 613, 380, 63, 1357, and 954 differentially expressed genes at hours 0, 2, 4, 8, 12 and 24 respectively. Pathway analysis revealed an initial upregulation in several immune/inflammatory pathways within the >=20% TBSA groups followed by shutdown. Severe burn injury is associated with an early proinflammatory immune response followed by shutdown of these pathways. Examination of the immunoinflammatory response to burn injury through differential gene regulation and associated immune pathways by injury severity may identify mechanistic targets for future intervention. Copyright (c) The Author(s) 2021. Published by Oxford University Press on behalf of the American Burn Association. All rights reserved. For permissions, please e-mail: [email protected].All authors: Campbell R, Carney BC, Detwiler L, Gautam A, Hammamieh R, Jett M, Keyloun JW, Miller SA, Moffatt LT, Shupp JW, SYSCOT study group, Yang ROriginally published: Journal of Burn Care & Research. 2021 Nov 15Fiscal year: FY2022Digital Object Identifier: Date added to catalog: 2022-01-25
Holdings
Item type Current library Collection Call number Status Date due Barcode
Journal Article MedStar Authors Catalog Article 34791339 Available 34791339

Available online through MWHC library: 2006 - present, Available in print through MWHC library: 2006 - present

Burn injury induces a systemic hyperinflammatory response with detrimental side effects. Studies have described the biochemical changes induced by severe burns, but the transcriptome response is not well characterized. The goal of this work is to characterize the blood transcriptome after burn injury. Burn patients presenting to a regional center between 2012-2017 were prospectively enrolled. Blood was collected on admission and at predetermined time points (hours 2, 4, 8, 12, 24). RNA was isolated and transcript levels were measured with a gene expression microarray. To identify differentially regulated genes (FDR<=0.1) by burn injury severity, patients were grouped by total body surface area (TBSA) above or below 20% and statistically enriched pathways were identified. Sixty-eight patients were analyzed, most patients were male with a median age of 41 (IQR, 30.5-58.5) years, and TBSA of 20% (11-34%). Thirty-five patients had %TBSA injury >=20%, and this group experienced greater mortality (26% vs. 3%, p=0.008). Comparative analysis of genes from patients with </>=20% TBSA revealed 1505, 613, 380, 63, 1357, and 954 differentially expressed genes at hours 0, 2, 4, 8, 12 and 24 respectively. Pathway analysis revealed an initial upregulation in several immune/inflammatory pathways within the >=20% TBSA groups followed by shutdown. Severe burn injury is associated with an early proinflammatory immune response followed by shutdown of these pathways. Examination of the immunoinflammatory response to burn injury through differential gene regulation and associated immune pathways by injury severity may identify mechanistic targets for future intervention. Copyright (c) The Author(s) 2021. Published by Oxford University Press on behalf of the American Burn Association. All rights reserved. For permissions, please e-mail: [email protected].

English

Powered by Koha