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Human iPSC-MSCs prevent steroid-resistant neutrophilic airway inflammation via modulating Th17 phenotypes

Overview of attention for article published in Stem Cell Research & Therapy, May 2018
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Title
Human iPSC-MSCs prevent steroid-resistant neutrophilic airway inflammation via modulating Th17 phenotypes
Published in
Stem Cell Research & Therapy, May 2018
DOI 10.1186/s13287-018-0897-y
Pubmed ID
Authors

Shu-Bin Fang, Hong-Yu Zhang, Ai-Yun Jiang, Xing-Liang Fan, Yong-Dong Lin, Cheng-Lin Li, Cong Wang, Xiang-Ci Meng, Qing-Ling Fu

Abstract

Human induced pluripotent stem cells-derived mesenchymal stem cells (iPSC-MSCs) have been shown to be effective in Type 2 helper T cells (Th2)-dominant eosinophilic allergic airway inflammation. However, the role of iPSC-MSCs in Type 17 helper T cells (Th17)-dominant neutrophilic airway inflammation remains poorly studied. Therefore, this study was to explore the effects of iPSC-MSCs on an experimental mouse model of steroid-resistant neutrophilic airway inflammation and further determine the underlying mechanisms. A mouse model of neutrophilic airway inflammation was established using ovalbumin (OVA) and lipopolysaccharide (LPS). Human iPSC-MSCs were systemically administered, and the lungs or bronchoalveolar lavage fluids (BALF) were collected at 4 h and 48 h post-challenge. The pathology and inflammatory cell infiltration, the T helper cells, T helper cells-associated cytokines, nuclear transcription factors and possible signaling pathways were evaluated. Human CD4+ T cells were polarized to T helper cells and the effects of iPSC-MSCs on the differentiation of T helper cells were determined. We successfully induced the mouse model of Th17 dominant neutrophilic airway inflammation. Human iPSC-MSCs but not dexamethasone significantly prevented the neutrophilic airway inflammation and decreased the levels of Th17 cells, IL-17A and p-STAT3. The mRNA levels of Gata3 and RORγt were also decreased with the treatment of iPSC-MSCs. We further confirmed the suppressive effects of iPSC-MSCs on the differentiation of human T helper cells. iPSC-MSCs showed therapeutic potentials in neutrophilic airway inflammation through the regulation on Th17 cells, suggesting that the iPSC-MSCs could be applied in the therapy for the asthma patients with steroid-resistant neutrophilic airway inflammation.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 20 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 20 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 5 25%
Student > Bachelor 3 15%
Student > Ph. D. Student 3 15%
Student > Doctoral Student 1 5%
Researcher 1 5%
Other 1 5%
Unknown 6 30%
Readers by discipline Count As %
Immunology and Microbiology 5 25%
Biochemistry, Genetics and Molecular Biology 4 20%
Agricultural and Biological Sciences 2 10%
Nursing and Health Professions 1 5%
Pharmacology, Toxicology and Pharmaceutical Science 1 5%
Other 2 10%
Unknown 5 25%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. 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 29 May 2018.
All research outputs
#20,514,440
of 23,081,466 outputs
Outputs from Stem Cell Research & Therapy
#2,070
of 2,437 outputs
Outputs of similar age
#289,998
of 330,379 outputs
Outputs of similar age from Stem Cell Research & Therapy
#58
of 66 outputs
Altmetric has tracked 23,081,466 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,437 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.1. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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We're also able to compare this research output to 66 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.