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Enhanced glycolysis contributes to the pathogenesis of experimental autoimmune neuritis

Overview of attention for article published in Journal of Neuroinflammation, February 2018
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Title
Enhanced glycolysis contributes to the pathogenesis of experimental autoimmune neuritis
Published in
Journal of Neuroinflammation, February 2018
DOI 10.1186/s12974-018-1095-7
Pubmed ID
Authors

Ru-Tao Liu, Min Zhang, Chun-Lin Yang, Peng Zhang, Na Zhang, Tong Du, Meng-Ru Ge, Long-Tao Yue, Xiao-Li Li, Heng Li, Rui-Sheng Duan

Abstract

With the recognition of the key roles of cellular metabolism in immunity, targeting metabolic pathway becomes a new strategy for autoimmune disease treatment. Guillain-Barré syndrome (GBS) is an acute immune-mediated inflammatory demyelinating disease of the peripheral nervous system, characterized by inflammatory cell infiltration. These inflammatory cells, including activated macrophages, Th1 cells, and Th17 cells, generally undergo metabolic reprogramming and rely mainly on glycolysis to exert functions. This study aimed to explore whether enhanced glycolysis contributed to the pathogenesis of experimental autoimmune neuritis (EAN), a classic model of GBS. Preventive and therapeutic treatments with glycolysis inhibitor, 2-deoxy-D-glucose (2-DG), were applied to EAN rats. The effects of treatments were determined by clinical scoring, weighting, and tissue examination. Flow cytometry and ELISA were used to evaluate T cell differentiation, autoantibody level, and macrophage functions in vivo and in vitro. Glycolysis inhibition with 2-DG not only inhibited the initiation, but also prevented the progression of EAN, evidenced by the improved clinical scores, weight loss, inflammatory cell infiltration, and demyelination of sciatic nerves. 2-DG inhibited the differentiation of Th1, Th17, and Tfh cells but enhanced Treg cell development, accompanied with reduced autoantibody secretion. Further experiments in vitro proved glycolysis inhibition decreased the nitric oxide production and phagocytosis of macrophages and suppressed the maturation of dendritic cells (DC). The effects of glycolysis inhibition on both innate and adaptive immune responses and the alleviation of animal clinical symptoms indicated that enhanced glycolysis contributed to the pathogenesis of EAN. Glycolysis inhibition may be a new therapy for GBS.

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The data shown below were collected from the profiles of 3 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 43 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 43 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 10 23%
Student > Bachelor 6 14%
Student > Doctoral Student 4 9%
Researcher 4 9%
Student > Master 3 7%
Other 6 14%
Unknown 10 23%
Readers by discipline Count As %
Medicine and Dentistry 6 14%
Biochemistry, Genetics and Molecular Biology 5 12%
Agricultural and Biological Sciences 4 9%
Immunology and Microbiology 4 9%
Nursing and Health Professions 3 7%
Other 9 21%
Unknown 12 28%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 06 March 2018.
All research outputs
#13,889,808
of 23,025,074 outputs
Outputs from Journal of Neuroinflammation
#1,506
of 2,655 outputs
Outputs of similar age
#177,789
of 331,231 outputs
Outputs of similar age from Journal of Neuroinflammation
#35
of 69 outputs
Altmetric has tracked 23,025,074 research outputs across all sources so far. This one is in the 38th percentile – i.e., 38% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,655 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.6. This one is in the 42nd percentile – i.e., 42% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 331,231 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 45th percentile – i.e., 45% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 69 others from the same source and published within six weeks on either side of this one. This one is in the 46th percentile – i.e., 46% of its contemporaries scored the same or lower than it.