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Silencing airway epithelial cell-derived hepcidin exacerbates sepsis-induced acute lung injury

Overview of attention for article published in Critical Care, August 2014
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Title
Silencing airway epithelial cell-derived hepcidin exacerbates sepsis-induced acute lung injury
Published in
Critical Care, August 2014
DOI 10.1186/s13054-014-0470-8
Pubmed ID
Authors

Qi Xing Chen, Sheng Wen Song, Qing Hua Chen, Cong Li Zeng, Xia Zheng, Jun Lu Wang, Xiang Ming Fang

Abstract

IntroductionThe production of antimicrobial peptides by airway epithelial cells is an important component of the innate immune response to pulmonary infection and inflammation. Hepcidin is a ß-defensin-like antimicrobial peptide and acts as a principal iron regulatory hormone. Hepcidin is mostly produced by hepatocytes, but is also expressed by other cells, such as airway epithelial cells. However, nothing is known about its function in lung infectious and inflammatory diseases. We therefore sought to investigate the role of airway epithelial cell-derived hepcidin in sepsis-induced acute lung injury.MethodsAcute lung injury was induced by polymicrobial sepsis via cecal ligation and puncture (CLP) surgery. Adenovirus-mediated short hairpin RNA specific for the mouse hepcidin gene hepc1 and control adenovirus were intratracheally injected into mice. The adenovirus-mediated knockdown of hepcidin in airway epithelial cells was evaluated in vivo. Lung injury and the 7-day survival rate were assessed. The levels of hepcidin-related iron export protein ferroportin were measured, and the iron content and function of alveolar macrophages were evaluated.ResultsThe hepcidin level in airway epithelial cells was upregulated during polymicrobial sepsis. The knockdown of airway epithelial cell-derived hepcidin aggravated the polymicrobial sepsis-induced lung injury and pulmonary bacterial infection and increased the mortality (53.33% in Ad-shHepc1 treated mice versus 12.5% in Ad-shNeg treated mice, P <0.05). The knockdown of hepcidin in airway epithelial cells also led to reduced ferroportin degradation and a low intracellular iron content in alveolar macrophages. Moreover, alveolar macrophages form the airway epithelial cell-derived hepcidin knockdown mice showed impaired phagocytic ability than those from the control mice.ConclusionsAirway epithelial cell-derived hepcidin plays an important role in CLP induced acute lung injury. The severe lung injury in the airway epithelial cell-derived hepcidin knockdown mice is at least partially related to the altered intracellular iron level and function of alveolar macrophages.

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The data shown below were collected from the profiles of 2 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 40 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Romania 1 3%
Canada 1 3%
Brazil 1 3%
Unknown 37 93%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 8 20%
Student > Master 8 20%
Researcher 5 13%
Student > Bachelor 4 10%
Student > Postgraduate 2 5%
Other 6 15%
Unknown 7 18%
Readers by discipline Count As %
Medicine and Dentistry 20 50%
Agricultural and Biological Sciences 3 8%
Chemistry 2 5%
Immunology and Microbiology 2 5%
Business, Management and Accounting 1 3%
Other 4 10%
Unknown 8 20%
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 17 September 2015.
All research outputs
#19,944,091
of 25,373,627 outputs
Outputs from Critical Care
#5,876
of 6,554 outputs
Outputs of similar age
#166,565
of 241,613 outputs
Outputs of similar age from Critical Care
#103
of 118 outputs
Altmetric has tracked 25,373,627 research outputs across all sources so far. This one is in the 18th percentile – i.e., 18% of other outputs scored the same or lower than it.
So far Altmetric has tracked 6,554 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 20.8. This one is in the 8th percentile – i.e., 8% 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 241,613 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 26th percentile – i.e., 26% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 118 others from the same source and published within six weeks on either side of this one. This one is in the 9th percentile – i.e., 9% of its contemporaries scored the same or lower than it.