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Neuropeptide regulation of adaptive immunity in the tibia fracture model of complex regional pain syndrome

Overview of attention for article published in Journal of Neuroinflammation, April 2018
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Title
Neuropeptide regulation of adaptive immunity in the tibia fracture model of complex regional pain syndrome
Published in
Journal of Neuroinflammation, April 2018
DOI 10.1186/s12974-018-1145-1
Pubmed ID
Authors

Wen-Wu Li, Tian-Zhi Guo, Xiaoyou Shi, Frank Birklein, Tanja Schlereth, Wade S. Kingery, J. David Clark

Abstract

Both dysfunctional neuropeptide signaling and immune system activation are characteristic of complex regional pain syndrome (CRPS). Unknown is whether substance P (SP) or calcitonin gene-related peptide (CGRP) support autoantibody production and, consequently, nociceptive sensitization. These experiments involved the use of a well-characterized tibia fracture model of CRPS. Mice deficient in SP expression (Tac1-/-) and CGRP signaling (RAMP1-/-) were used to probe the neuropeptide dependence of post-fracture sensitization and antibody production. The deposition of IgM in the spinal cord, sciatic nerves, and skin was followed using Western blotting, as was expression of the CRPS-related autoantigen cytokeratin 16 (Krt16). Passive serum transfer to B-cell-deficient muMT mice was used to assess the production of functional autoantibodies in CRPS model mice. The use of immunohistochemistry allowed us to assess neuropeptide-containing fiber distribution and Langerhans cell abundance in mouse and human CRPS patient skin, while Langerhans cell-deficient mice were used to assess the functional contributions of these cells. Functional SP and CGRP signaling were required both for the full development of nociceptive sensitization after fracture and the deposition of IgM in skin and neural tissues. Furthermore, the passive transfer of serum from wildtype but not neuropeptide-deficient mice to fractured muMT mice caused enhanced allodynia and postural unweighting. Langerhans cells were increased in number in the skin of fracture mice and CRPS patients, and those increases in mice were reduced in neuropeptide signaling-deficient animals. Unexpectedly, Langerhans cell-deficient mice showed normal nociceptive sensitization after fracture. However, the increased expression of Krt16 after tibia fracture was not seen in neuropeptide-deficient mice. Collectively, these data support the hypothesis that neuropeptide signaling in the fracture limb of mice is required for autoantigenic IgM production and nociceptive sensitization. The mechanism may be related to neuropeptide-supported autoantigen expression.

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Mendeley readers

The data shown below were compiled from readership statistics for 21 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 21 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 3 14%
Professor > Associate Professor 2 10%
Student > Ph. D. Student 2 10%
Student > Bachelor 2 10%
Student > Doctoral Student 1 5%
Other 4 19%
Unknown 7 33%
Readers by discipline Count As %
Medicine and Dentistry 5 24%
Neuroscience 4 19%
Pharmacology, Toxicology and Pharmaceutical Science 2 10%
Sports and Recreations 1 5%
Agricultural and Biological Sciences 1 5%
Other 1 5%
Unknown 7 33%

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 13 April 2018.
All research outputs
#11,386,366
of 12,802,184 outputs
Outputs from Journal of Neuroinflammation
#1,257
of 1,477 outputs
Outputs of similar age
#239,174
of 274,107 outputs
Outputs of similar age from Journal of Neuroinflammation
#20
of 23 outputs
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