Evidence map›Paper›PMID 36050760›Full record

ArticleExperimental hematology & oncology2022

Impaired mitochondria of Tregs decreases OXPHOS-derived ATP in primary immune thrombocytopenia with positive plasma pathogens detected by metagenomic sequencing.

Yanxia Zhan, Jingjing Cao, Lili Ji, Miaomiao Zhang, Qi Shen, Pengcheng Xu, Xibing Zhuang, Shanshan Qin, Fanli Hua, Lihua Sun and 3 more

Abstract read
In one paragraph

Article in Experimental hematology & oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Yanxia Zhan *Department of Hematology, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China.
Jingjing Cao *Department of Hematology, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China.
Lili JiDepartment of Hematology, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China.
Miaomiao ZhangInstitute of Clinical Science, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Qi ShenInstitute of Clinical Science, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Pengcheng XuDepartment of Hematology, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China.
Xibing ZhuangDepartment of Hematology, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China.
Shanshan QinDepartment of Hematology, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China.
Fanli HuaDepartment of Hematology, Zhongshan Hospital Qingpu Branch, Fudan University, Shanghai, 201700, China.
Lihua SunDepartment of Hematology, Zhongshan Hospital Qingpu Branch, Fudan University, Shanghai, 201700, China.
Feng LiDepartment of Hematology, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China.
Hao ChenDepartment of Thoracic Surgery, Zhongshan Hospital Xuhui Branch, Fudan University, 966 Mid Huaihai Rd, Shanghai, 200031, China. h.chen@fudan.edu.cn.
Yunfeng ChengDepartment of Hematology, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China. yfcheng@fudan.edu.cn.

Funding

Key Subject Construction Program of Shanghai Health Administrative Authority ZK2019B30National Natural Science Foundation of China 81500090National Natural Science Foundation of China 81878898Program of the Shanghai Academic/Technology Researcher leader 20XD1401000Science and Technology Commission of Shanghai Municipality 21ZR1459000Shanghai Engineering Research Center of Tumor Multi-Target Gene Diagnosis 20DZ2254300
6 · The paper itself

Abstract

backgroundPrimary immune thrombocytopenia (ITP) is an autoimmune disease. Some ITP patients are associated with pathogen infection undetected with conventional technologies. Investigating the changes of T cells and potential metabolic mechanism are important for better understanding of ITP.

methodsThe study enrolled 75 newly diagnosed ITP patients. The pathogens of patients were detected by metagenomic next-generation sequencing (mNGS). Plasma lipids were measured by liquid chromatography-mass spectrometry (LC-MS). CD4 T cell and CD8 T cell were analyzed using flow cytometry. Mitochondrial reactive oxygen species (ROS) and mitochondrial membrane potential were measured by flow cytometry. Seahorse XF real-time ATP rate assay was used to investigate the change of cellular metabolism.

resultsPositive plasma pathogens were detected in seven ITP patients. Of them, 5 (71.4%) positive pathogen-ITP patients were no response (NR) after first-line treatment with corticosteroids. Regulatory T cells (Tregs) increased significantly in positive pathogen-ITP patients compared to negative pathogen-ITP patients and healthy controls (HC). Mitochondrial membrane potential of Th17 and Tregs were decreased in positive pathogen-ITP and negative pathogen-ITP patients, compared to HC (all p < 0.05). The overall metabolism flux of positive pathogen-ITP patients was decreased, as compared to HC (p = 0.004), of them a higher proportion of glycolysis-derived ATP and a smaller proportion of oxidative phosphorylation (OXPHOS)-derived ATP were found in Tregs. The ATP rate index of Tregs was decreased significantly in positive pathogen-ITP patients compared to negative pathogen-ITP patients and HC (p < 0.05).

conclusionsImpaired mitochondria function of Tregs in positive pathogen-ITP patients caused a decrease of OXPHOS-derived ATP and overall metabolism flux that might be the cause of steroid resistance in ITP patients.

Indexed as

GlycolysisImmune thrombocytopeniaOxidative phosphorylationPathogensTregs (Regulatory T cells)

Identifiers

PMID36050760
PMCPMC9434515

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.