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Th-17 regulatory cytokines inhibit corticosteroid induced airway structural cells apoptosis

Overview of attention for article published in Respiratory Research, January 2016
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (88th percentile)
  • High Attention Score compared to outputs of the same age and source (85th percentile)

Mentioned by

news
1 news outlet
twitter
2 tweeters
facebook
1 Facebook page
googleplus
1 Google+ user

Citations

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15 Dimensions

Readers on

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14 Mendeley
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Title
Th-17 regulatory cytokines inhibit corticosteroid induced airway structural cells apoptosis
Published in
Respiratory Research, January 2016
DOI 10.1186/s12931-015-0307-2
Pubmed ID
Authors

Rabih Halwani, Asma Sultana, Roua Al-Kufaidy, Amer Jamhawi, Alejandro Vazquez-Tello, Saleh Al-Muhsen

Abstract

Although corticosteroid is a powerful anti-inflammatory drug that is used widely to control asthma, still severe asthmatics can develop steroid resistance. Airway fibroblasts are quite resistant to steroids during Idiopathic pulmonary fibrosis (IPF) and fibrosis in asthmatic lungs is not always controlled. Th-17 regulatory cytokine which are elevated in lung tissues of asthmatics were shown to enhance the survival of various types of cells. STAT factors are central to this anti-apoptotic function. However, it is not yet clear whether these cytokines contribute to steroid hypo-responsiveness in asthma. Therefore, in this study, we investigated the ability of Th-17 regulatory cytokines, specifically IL-21, IL22 and IL23, to protect structural airway cells against dexamethasone-induced apoptosis. Primary human fibroblasts, ASM cells, and lung endothelial cells line were treated with IL-21, IL-22, and IL-23 cytokines before incubation with dexamethasone and the level of apoptosis was determined by measuring cellular Annexin-V using Flow cytometry. Our data indicated that treatment with Th-17 regulatory cytokines was effective in inhibiting induced apoptosis for both fibroblasts and endothelial cells but not ASM cells. STAT3 phosphorylation levels were also upregulated in fibroblasts and endothelial upon treatment with these cytokines. Interestingly, inhibiting STAT3 phosphorylation abrogated IL-21, IL-22, and IL-23 anti-apoptotic effect on fibroblasts and endothelial cells. This data suggest that Th-17 regulatory cytokines may play a critical role in regulating the survival of fibroblasts during asthma, IPF as well as other chronic lung inflammatory diseases leading to enhanced fibrosis. Accordingly, findings of this paper may pave the way for more extensive research on the role of these regulatory cytokines in fibrosis development in various chronic inflammatory diseases.

Twitter Demographics

The data shown below were collected from the profiles of 2 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 14 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Brazil 1 7%
Unknown 13 93%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 4 29%
Other 3 21%
Researcher 2 14%
Student > Doctoral Student 1 7%
Librarian 1 7%
Other 2 14%
Unknown 1 7%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 3 21%
Immunology and Microbiology 3 21%
Pharmacology, Toxicology and Pharmaceutical Science 1 7%
Business, Management and Accounting 1 7%
Computer Science 1 7%
Other 3 21%
Unknown 2 14%

Attention Score in Context

This research output has an Altmetric Attention Score of 12. 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 26 September 2020.
All research outputs
#1,996,476
of 18,957,622 outputs
Outputs from Respiratory Research
#210
of 2,355 outputs
Outputs of similar age
#41,493
of 354,820 outputs
Outputs of similar age from Respiratory Research
#4
of 20 outputs
Altmetric has tracked 18,957,622 research outputs across all sources so far. Compared to these this one has done well and is in the 89th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 2,355 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 7.0. This one has done particularly well, scoring higher than 90% of its peers.
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 354,820 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 88% of its contemporaries.
We're also able to compare this research output to 20 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 85% of its contemporaries.