Association between microbiome and the development of adverse posttraumatic neuropsychiatric sequelae after traumatic stress exposure.
Association between microbiome and the development of adverse posttraumatic neuropsychiatric sequelae after traumatic stress exposure.
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DOI：
10.1038/s41398-023-02643-8
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发表时间：
2023-11-18
影响因子：
6.8
通讯作者：
Haran, John P.
中科院分区：
文献类型：
--
作者：
Zeamer, Abigail L.;Salive, Marie-Claire;An, Xinming;Beaudoin, Francesca L.;House, Stacey L.;Stevens, Jennifer S.;Zeng, Donglin;Neylan, Thomas C.;Clifford, Gari D.;Linnstaedt, Sarah D.;Rauch, Scott L.;Storrow, Alan B.;Lewandowski, Christopher;Musey, Paul I., Jr.;Hendry, Phyllis L.;Sheikh, Sophia;Jones, Christopher W.;Punches, Brittany E.;Swor, Robert A.;Hudak, Lauren A.;Pascual, Jose L.;Seamon, Mark J.;Harris, Erica;Pearson, Claire;Peak, David A.;Merchant, Roland C.;Domeier, Robert M.;Rathlev, Niels K.;O'Neil, Brian J.;Sergot, Paulina;Sanchez, Leon D.;Bruce, Steven E.;Kessler, Ronald C.;Koenen, Karestan C.;McLean, Samuel A.;Bucci, Vanni;Haran, John P.
遭受创伤的患者经常会出现不良的创伤后神经精神后遗症（APNS）。目前尚不清楚促进 APNS 的生物学机制，但微生物群-肠-脑轴提供了理解机制和干预可能性的途径。创伤暴露后的微生物组组成对于神经精神结果的研究很少。我们的目的是确定发生 APNS 的急诊室创伤患者的肠道微生物组是否具有功能失调的肠道微生物组特征，并发现潜在的相关机制。我们对参加“促进创伤后恢复理解”(AURORA) 研究的一部分成年人的粪便样本 (n = 51) 进行了宏基因组分析。收集创伤后应激障碍 (PTSD) 的创伤后两周、八周和十二周结果（DSM-5 的 PTSD 检查表）、标准化抑郁评分（PROMIS 抑郁简表 8b）和躯体症状计数。使用微生物丰度和相关人口统计数据为每个结果创建广义线性模型。使用混合效应随机森林机器学习模型来识别 APNS 结果与微生物特征之间的关联，并从粪便宏基因组中编码代谢途径。研究发现，微生物物种，包括普氏黄酮、侏儒瘤胃球菌和双歧杆菌，是常见的肠道共生微生物，对于根据微生物丰度数据预测更差的 APNS 结果非常重要。值得注意的是，通过使用微生物代谢途径的 APNS 结果模型，通过减少 L-精氨酸相关途径基因和增加瓜氨酸和鸟氨酸途径，可以高度预测更差的 APNS 结果。常见的共生微生物种类在发生 APNS 的个体中丰富。更值得注意的是，我们确定了肠道微生物组降低整体精氨酸生物利用度的生物学机制，这种代谢变化也在创伤后应激障碍患者的血浆中得到了证实。
Patients exposed to trauma often experience high rates of adverse post-traumatic neuropsychiatric sequelae (APNS). The biological mechanisms promoting APNS are currently unknown, but the microbiota-gut-brain axis offers an avenue to understanding mechanisms as well as possibilities for intervention. Microbiome composition after trauma exposure has been poorly examined regarding neuropsychiatric outcomes. We aimed to determine whether the gut microbiomes of trauma-exposed emergency department patients who develop APNS have dysfunctional gut microbiome profiles and discover potential associated mechanisms. We performed metagenomic analysis on stool samples (n = 51) from a subset of adults enrolled in the Advancing Understanding of RecOvery afteR traumA (AURORA) study. Two-, eight- and twelve-week post-trauma outcomes for post-traumatic stress disorder (PTSD) (PTSD checklist for DSM-5), normalized depression scores (PROMIS Depression Short Form 8b) and somatic symptom counts were collected. Generalized linear models were created for each outcome using microbial abundances and relevant demographics. Mixed-effect random forest machine learning models were used to identify associations between APNS outcomes and microbial features and encoded metabolic pathways from stool metagenomics. Microbial species, including Flavonifractor plautii, Ruminococcus gnavus and, Bifidobacterium species, which are prevalent commensal gut microbes, were found to be important in predicting worse APNS outcomes from microbial abundance data. Notably, through APNS outcome modeling using microbial metabolic pathways, worse APNS outcomes were highly predicted by decreased L-arginine related pathway genes and increased citrulline and ornithine pathways. Common commensal microbial species are enriched in individuals who develop APNS. More notably, we identified a biological mechanism through which the gut microbiome reduces global arginine bioavailability, a metabolic change that has also been demonstrated in the plasma of patients with PTSD.
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影响因子：
5.2
作者：
Bradley, Evan S.;Zeamer, Abigail L.;Bucci, Vanni;Cincotta, Lindsey;Salive, Marie-Claire;Dutta, Protiva;Mutaawe, Shafik;Anya, Otuwe;Tocci, Christopher;Moormann, Ann;Ward, Doyle V.;McCormick, Beth A.;Haran, John P.
通讯作者：
Haran, John P.
影响因子：
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通讯作者：
Segata N
DOI：
10.1093/gerona/glab167
发表时间：
2021-06-14
影响因子：
5.1
作者：
Haran, John P.;Zeamer, Abigail;McCormick, Beth A.
通讯作者：
McCormick, Beth A.
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