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A pathogenic role for tumor necrosis factor-related apoptosis-inducing ligand in chronic obstructive pulmonary disease

Overview of attention for article published in Mucosal Immunology (1933-0219), November 2015
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  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (91st percentile)
  • High Attention Score compared to outputs of the same age and source (85th percentile)

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2 news outlets
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3 X users

Citations

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63 Dimensions

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49 Mendeley
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Title
A pathogenic role for tumor necrosis factor-related apoptosis-inducing ligand in chronic obstructive pulmonary disease
Published in
Mucosal Immunology (1933-0219), November 2015
DOI 10.1038/mi.2015.111
Pubmed ID
Authors

T J Haw, M R Starkey, P M Nair, S Pavlidis, G Liu, D H Nguyen, A C Hsu, I Hanish, R Y Kim, A M Collison, M D Inman, P A Wark, P S Foster, D A Knight, J Mattes, H Yagita, I M Adcock, J C Horvat, P M Hansbro

Abstract

Chronic obstructive pulmonary disease (COPD) is a life-threatening inflammatory respiratory disorder, often induced by cigarette smoke (CS) exposure. The development of effective therapies is impaired by a lack of understanding of the underlining mechanisms. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a cytokine with inflammatory and apoptotic properties. We interrogated a mouse model of CS-induced experimental COPD and human tissues to identify a novel role for TRAIL in COPD pathogenesis. CS exposure of wild-type mice increased TRAIL and its receptor messenger RNA (mRNA) expression and protein levels, as well as the number of TRAIL(+)CD11b(+) monocytes in the lung. TRAIL and its receptor mRNA were also increased in human COPD. CS-exposed TRAIL-deficient mice had decreased pulmonary inflammation, pro-inflammatory mediators, emphysema-like alveolar enlargement, and improved lung function. TRAIL-deficient mice also developed spontaneous small airway changes with increased epithelial cell thickness and collagen deposition, independent of CS exposure. Importantly, therapeutic neutralization of TRAIL, after the establishment of early-stage experimental COPD, reduced pulmonary inflammation, emphysema-like alveolar enlargement, and small airway changes. These data provide further evidence for TRAIL being a pivotal inflammatory factor in respiratory diseases, and the first preclinical evidence to suggest that therapeutic agents that target TRAIL may be effective in COPD therapy.Mucosal Immunology advance online publication, 11 November 2015; doi:10.1038/mi.2015.111.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 49 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Germany 1 2%
Unknown 48 98%

Demographic breakdown

Readers by professional status Count As %
Researcher 8 16%
Student > Ph. D. Student 7 14%
Student > Bachelor 5 10%
Student > Doctoral Student 5 10%
Student > Master 4 8%
Other 11 22%
Unknown 9 18%
Readers by discipline Count As %
Medicine and Dentistry 10 20%
Agricultural and Biological Sciences 7 14%
Immunology and Microbiology 5 10%
Biochemistry, Genetics and Molecular Biology 4 8%
Nursing and Health Professions 4 8%
Other 10 20%
Unknown 9 18%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 21. 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 13 November 2019.
All research outputs
#1,810,974
of 26,184,649 outputs
Outputs from Mucosal Immunology (1933-0219)
#159
of 1,431 outputs
Outputs of similar age
#24,971
of 294,776 outputs
Outputs of similar age from Mucosal Immunology (1933-0219)
#5
of 34 outputs
Altmetric has tracked 26,184,649 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 93rd percentile: it's in the top 10% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 1,431 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 13.0. This one has done well, scoring higher than 88% 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 294,776 tracked outputs that were published within six weeks on either side of this one in any source. This one has done particularly well, scoring higher than 91% of its contemporaries.
We're also able to compare this research output to 34 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.