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Interleukin-6-dependent influence of nociceptive sensory neurons on antigen-induced arthritis

Overview of attention for article published in Arthritis Research & Therapy, 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 (85th percentile)
  • Good Attention Score compared to outputs of the same age and source (66th percentile)

Mentioned by

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1 news outlet
twitter
1 tweeter

Citations

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34 Dimensions

Readers on

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41 Mendeley
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Title
Interleukin-6-dependent influence of nociceptive sensory neurons on antigen-induced arthritis
Published in
Arthritis Research & Therapy, November 2015
DOI 10.1186/s13075-015-0858-0
Pubmed ID
Authors

Matthias Ebbinghaus, Gisela Segond von Banchet, Julia Massier, Mieczyslaw Gajda, Rolf Bräuer, Michaela Kress, Hans-Georg Schaible

Abstract

Interleukin-6 (IL-6) is an important mediator of inflammation. In addition to cells involved in inflammation, sensory nociceptive neurons express the IL-6 signal-transducer glycoprotein 130 (gp130). These neurons are not only involved in pain generation but also produce neurogenic inflammation by release of neuropeptides such as calcitonin gene-related peptide (CGRP). Whether IL-6 activation of sensory neurons contributes to the induction of inflammation is unknown. This study explored whether the action of IL-6 on sensory neurons plays a role in the generation of neurogenic inflammation and arthritis induction. In SNS-gp130(-/-) mice lacking gp130 selectively in sensory neurons and appropriate control littermates (SNS-gp130(flox/flox)), we induced antigen-induced arthritis (AIA), and assessed swelling, histopathological arthritis scores, pain scores, expression of CGRP in sensory neurons, serum concentrations of CGRP and cytokines, and the cytokine release from single cell suspensions from lymph nodes and spleens. In wild-type mice CGRP release was determined during development of AIA and, in cultured sensory neurons, upon IL-6 stimulation. Compared to SNS-gp130(flox/flox) mice SNS-gp130(-/-) mice showed significantly weaker initial swelling, reduced serum concentrations of CGRP, IL-6, and IL-2, no inflammation-evoked upregulation of CGRP in sensory neurons, but similar histopathological arthritis scores during AIA. During the initial swelling phase of AIA, CGRP was significantly increased in the serum, knee and spleen. In vitro, IL-6 augmented the release of CGRP from cultured sensory neurons. Upon antigen-specific restimulation lymphocytes from SNS-gp130(-/-) mice released more interleukin-17 and interferon-γ than lymphocytes from SNS-gp130(flox/flox) mice. In naive lymphocytes from SNS-gp130(flox/flox) and SNS-gp130(-/-) mice CGRP reduced the release of IL-2 (a cytokine which inhibits the release of interleukin-17 and interferon-γ). IL-6 signaling in sensory neurons plays a role in the expression of arthritis. Selective deletion of gp130 signaling in sensory neurons reduces the swelling of the joint (most likely by reducing neurogenic inflammation) but increases some proinflammatory systemic cellular responses such as the release of interleukin-17 and interferon-γ from lymphocytes upon antigen-specific restimulation. Thus IL-6 signaling in sensory neurons is not only involved in pain generation but also in the coordination of the inflammatory response.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter 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 41 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 2 5%
Germany 1 2%
Unknown 38 93%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 10 24%
Researcher 6 15%
Professor 5 12%
Student > Doctoral Student 4 10%
Other 3 7%
Other 6 15%
Unknown 7 17%
Readers by discipline Count As %
Medicine and Dentistry 9 22%
Agricultural and Biological Sciences 5 12%
Neuroscience 5 12%
Pharmacology, Toxicology and Pharmaceutical Science 4 10%
Immunology and Microbiology 2 5%
Other 7 17%
Unknown 9 22%

Attention Score in Context

This research output has an Altmetric Attention Score of 10. 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 22 November 2015.
All research outputs
#1,432,593
of 12,451,992 outputs
Outputs from Arthritis Research & Therapy
#398
of 1,983 outputs
Outputs of similar age
#48,240
of 336,989 outputs
Outputs of similar age from Arthritis Research & Therapy
#91
of 288 outputs
Altmetric has tracked 12,451,992 research outputs across all sources so far. Compared to these this one has done well and is in the 88th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 1,983 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.0. This one has done well, scoring higher than 82% 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 336,989 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 85% of its contemporaries.
We're also able to compare this research output to 288 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 66% of its contemporaries.