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Angiotensin-(1-7) Promotes Resolution of Neutrophilic Inflammation in a Model of Antigen-Induced Arthritis in Mice

Overview of attention for article published in Frontiers in immunology, November 2017
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Title
Angiotensin-(1-7) Promotes Resolution of Neutrophilic Inflammation in a Model of Antigen-Induced Arthritis in Mice
Published in
Frontiers in immunology, November 2017
DOI 10.3389/fimmu.2017.01596
Pubmed ID
Authors

Lívia C. Barroso, Giselle S. Magalhaes, Izabela Galvão, Alessandra C. Reis, Daniella G. Souza, Lirlândia P. Sousa, Robson A. S. Santos, Maria Jose Campagnole-Santos, Vanessa Pinho, Mauro Martins Teixeira

Abstract

Defective resolution of inflammation may be crucial for the initiation and development of chronic inflammatory diseases, such as arthritis. Therefore, it has been suggested that therapeutic strategies based on molecules that facilitate inflammation resolution present great potential for the treatment of chronic inflammatory diseases. In this study, we investigated the effects and role of angiotensin-(1-7) [Ang-(1-7)] in driving resolution of neutrophilic inflammation in a model of arthritis. For this purpose, male C57BL/6 mice were subjected to antigen-induced arthritis and treated with Ang-(1-7) at the peak of the inflammatory process. Analysis of the number of inflammatory cells, apoptosis, and immunofluorescence for NF-κB was performed in the exudate collected from the knee cavity. Neutrophil accumulation in periarticular tissue was measured by assaying myeloperoxidase activity. Apoptosis of human neutrophil after treatment with Ang-(1-7) was evaluated morphologically and by flow cytometry, and NF-κB phosphorylation by immunofluorescence. Efferocytosis was evaluated in vivo. Therapeutic treatment with Ang-(1-7) at the peak of inflammation promoted resolution, an effect associated with caspase-dependent neutrophils apoptosis and NF-κB inhibition. Importantly, Ang-(1-7) was also able to induce apoptosis of human neutrophils, an effect associated with NF-κB inhibition. The pro-resolving effects of Ang-(1-7) were inhibited by the Mas receptor antagonist A779. Finally, we showed that Ang-(1-7) increased the efferocytic ability of murine macrophages. Our results clearly demonstrate that Ang-(1-7) resolves neutrophilic inflammation in vivo acting in two key step of resolution: apoptosis of neutrophils and their removal by efferocytosis. Ang-(1-7) is a novel mediator of resolution of inflammation.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 44 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 44 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 6 14%
Researcher 5 11%
Student > Master 5 11%
Student > Bachelor 4 9%
Student > Postgraduate 3 7%
Other 7 16%
Unknown 14 32%
Readers by discipline Count As %
Immunology and Microbiology 11 25%
Biochemistry, Genetics and Molecular Biology 5 11%
Medicine and Dentistry 5 11%
Agricultural and Biological Sciences 4 9%
Pharmacology, Toxicology and Pharmaceutical Science 3 7%
Other 2 5%
Unknown 14 32%
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 27 December 2017.
All research outputs
#17,292,294
of 25,382,440 outputs
Outputs from Frontiers in immunology
#20,307
of 31,537 outputs
Outputs of similar age
#279,467
of 445,134 outputs
Outputs of similar age from Frontiers in immunology
#399
of 567 outputs
Altmetric has tracked 25,382,440 research outputs across all sources so far. This one is in the 21st percentile – i.e., 21% of other outputs scored the same or lower than it.
So far Altmetric has tracked 31,537 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.4. This one is in the 28th percentile – i.e., 28% 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 445,134 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 28th percentile – i.e., 28% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 567 others from the same source and published within six weeks on either side of this one. This one is in the 22nd percentile – i.e., 22% of its contemporaries scored the same or lower than it.