Cited by 45Pain Mechanisms and TreatmentsStress Responses and CortisolNeuropeptides and Animal Physiology

Lifetime modulation of the pain system via neuroimmune and neuroendocrine interactions

Open access
Zouikr, Ihssane, Karshikoff, Bianka·2017·Frontiers in Immunology

Abstract

Chronic pain is a debilitating condition that still is challenging both clinicians and researchers. Despite intense research, it is still not clear why some individuals develop chronic pain while others do not or how to heal this disease. In this review, we argue for a multisystem approach to understand chronic pain. Pain is not only to be viewed simply as a result of aberrant neuronal activity but also as a result of adverse early-life experiences that impact an individual's endocrine, immune, and nervous systems and changes which in turn program the pain system. First, we give an overview of the ontogeny of the central nervous system, endocrine, and immune systems and their windows of vulnerability. Thereafter, we summarize human and animal findings from our laboratories and others that point to an important role of the endocrine and immune systems in modulating pain sensitivity. Taking "early-life history" into account, together with the past and current immunological and endocrine status of chronic pain patients, is a necessary step to understand chronic pain pathophysiology and assist clinicians in tailoring the best therapeutic approach.

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Crossref · 10.3389/fimmu.2017.00276

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  • Activated mast cells may establish a self-sustaining positive feedback of neuroinflammation and autoimmunity.

    “These activated mast cells may then go on to establish a self-sustaining positive feedback of neuroinflammation and autoimmunity70–72”

    From Leveraging Prior Knowledge of Endocrine Immune Regulation in the Therapeutically-relevant Phenotyping of Women with Chronic Fatigue Syndrome (2019) · cites this paper as [71]

    In “Animal Studies Demonstrate Inflammation-Induced Pain Sensitivity” (page unavailable), the paper says mast cells release pro-inflammatory cytokines and that peripheral inflammation can lead to central neuroinflammation. It does not describe a self-sustaining feedback loop or link mast-cell activation to autoimmunity. (LLM, conf=0.78)

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Research works printed but not linked: 1

  1. [218]Engler H Benson S Wegner A Spreitzer I Schedlowski M Elsenbruch S Men and women differ in inflammatory and neuroendocrine responses to endotoxin but not in the severity of sickness symptoms. Brain Behav Immun (2016) 52: 18– 26. 10.1016/j.bbi.2015.08.013 26291403 · DOI

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Authors
Zouikr, I., & Karshikoff, B.
Affiliations
  • RIKEN (JP)
  • Stockholm University (SE)
Corresponding author
Zouikr, Ihssane
Venue
Frontiers in Immunology
Published
2017-03-13
Volume
8
Pages
276-276
ISSN
1664-3224 (ISSN-L)
OpenAlex
W2596201282
Cited by
45
References
276
Citations by year
2026: 4 · 2025: 4 · 2024: 5 · 2023: 4 · 2022: 7 · 2021: 4 · 2020: 6 · 2019: 9 · 2018: 1 · 2017: 1
FWCI
0.57
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Frontiers in Immunology (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
Funders
Japan Society for the Promotion of Science (16F16726)
Topics
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
Keywords
chronic pain, neuroimmune interactions, neuroendocrine interaction, early life experience, pain sensitivity, immune system development, endocrine system development, window of vulnerability

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