Non-severe burns induce a prolonged systemic metabolic phenotype indicative of a persistent inflammatory response post-injury
bioRxiv (Cold Spring Harbor Laboratory)(2023)
摘要
Globally, burns are a significant cause of injury that can cause substantial acute trauma as well as lead to increased incidence of chronic co-morbidity and disease. To date, research has primarily focused on the systemic response to severe injury, with little in the literature reported on impact of non-severe injuries (<15% total burn surface area; TBSA). To elucidate the metabolic consequences of non-severe burn injury, longitudinal plasma was collected from adults (n=35) who presented at hospital with a non-severe burn injury at admission, and at 6 week follow up. A cross-sectional baseline sample was also collected from non-burn control participants (n=14). Samples underwent multiplatform metabolic phenotyping using 1H nuclear magnetic resonance spectroscopy and liquid chromatography-mass spectrometry to quantify 112 lipoprotein and glycoproteins signatures and 852 lipid species from across 20 subclasses.
Multivariate data modelling (Orthogonal projection to latent structures-discriminate analysis) revealed alterations in lipoprotein and lipid metabolism when comparing baseline control to hospital admission samples, with the phenotypic signature found to be sustained at follow up. Univariate (Mann-Whitney U) testing and OPLS-DA indicated specific increases in GlycB (p-value <1.0e-4), low density lipoprotein-2 subfractions (Variable importance in projection score; VIP >6.83e-1) and monoacyglyceride (20:4)(p-value <1.0e-4) and decreases in circulating anti-inflammatory high-density lipoprotein-4 subfractions (VIP >7.75e-1), phosphatidylcholines, phosphatidylglycerols, phosphatidylinositols and phosphatidylserines.
The results indicate a persistent systemic metabolic phenotype that occurs even in cases of non-severe burn injury. The phenotype is indicative of an acute inflammatory profile which continues to be sustained post-injury, suggesting an impact on systems health beyond the site of injury. The phenotypes contained metabolic signatures consistent with chronic inflammatory states reported to have elevated incidence post-burn injury. Such phenotypic signatures may provide patient stratification opportunities, to identify individual responses to injury, personalise intervention strategies and improve acute care, reducing risk of chronic co-morbidity.
### Competing Interest Statement
The authors have declared no competing interest.
* AB100
: Apolipoprotein B100
ABA1
: Apolipoprotein B100/apolipoprotein A1
B.I.-LISA
: Bruker IVDr lipoprotein subclass analysis
CABIN
: Randomised placebo-controlled trial of Celecoxib for acute burn inflammation
CER
: Ceramide
CV-AUROC
: Cross validated-area under the receiver operating characteristic
DAG
: Diacylglyceride
DIRE
: Diffusion and relaxation editing
FFA
: Free fatty acid
H4A1
: HDL-4 apolipoprotein A1
HDA1
: HDL-associated apolipoprotein A1
HDL
: High density lipoprotein
hs-CRP
: high sensitivity C-reactive protein
ILDL
: Intermediate low density lipoprotein
IVDr
: in vitro Diagnostics research
L2AB
: LDL-2-associated apolipoprotein B
LC-QQQ-MS
: Liquid chromatography-tandem mass spectrometry
LDL
: Low density lipoprotein
LPC
: Lysophosphatidylcholine
LPE
: Lysophosphatidylethanolamine
LPG
: Lysophosphatidylglycerol
MAG
: Monoacylglyceride
MS
: Mass spectrometry
NMR
: Nuclear magnetic resonance
OPLS-DA
: Supervised orthogonal projection to latent structures discriminant analysis
PC
: Phosphatidylcholine
PCA
: Principal component analysis
PE
: Phosphatidylethanolamine
PI
: Phosphatidylinositol
PG
: Phosphatidylglycerol
PS
: Phosphatidylserine
QC
: Quality control
RSD
: Relative standard deviation
SM
: Sphingomyelin
SPC
: Supramolecular phospholipid composite
TAG
: Triacylglyceride
TBSA
: Total burn surface area
TSP
: Sodium trimethylsilyl propionate-[2,2,3,3-2H4]
VIP
: Variable important in projection
VLDL
: Very low density lipoprotein
更多查看译文
AI 理解论文
溯源树
样例
生成溯源树,研究论文发展脉络
Chat Paper
正在生成论文摘要