喹啉酸
犬尿氨酸
犬尿氨酸途径
牛磺酸
新喋呤
生物
促炎细胞因子
代谢物
细胞因子
免疫学
趋化因子
代谢组
炎症
生物化学
色氨酸
氨基酸
作者
Nathan G. Lawler,Nicola Gray,Torben Kimhofer,Berin A. Boughton,Melvin Gay,Rongchang Yang,Aude-Claire Morillon,Sung‐Tong Chin,Monique Ryan,Sofina Begum,Sze-How Bong,Jérôme D. Coudert,Dale W. Edgar,Edward Raby,Sven Pettersson,Toby Richards,Elaine Holmes,Luke Whiley,Jeremy K. Nicholson
标识
DOI:10.1021/acs.jproteome.1c00052
摘要
We performed quantitative metabolic phenotyping of blood plasma in parallel with cytokine/chemokine analysis from participants who were either SARS-CoV-2 (+) (n = 10) or SARS-CoV-2 (-) (n = 49). SARS-CoV-2 positivity was associated with a unique metabolic phenotype and demonstrated a complex systemic response to infection, including severe perturbations in amino acid and kynurenine metabolic pathways. Nine metabolites were elevated in plasma and strongly associated with infection (quinolinic acid, glutamic acid, nicotinic acid, aspartic acid, neopterin, kynurenine, phenylalanine, 3-hydroxykynurenine, and taurine; p < 0.05), while four metabolites were lower in infection (tryptophan, histidine, indole-3-acetic acid, and citrulline; p < 0.05). This signature supports a systemic metabolic phenoconversion following infection, indicating possible neurotoxicity and neurological disruption (elevations of 3-hydroxykynurenine and quinolinic acid) and liver dysfunction (reduction in Fischer's ratio and elevation of taurine). Finally, we report correlations between the key metabolite changes observed in the disease with concentrations of proinflammatory cytokines and chemokines showing strong immunometabolic disorder in response to SARS-CoV-2 infection.
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