Acute inflammatory response via neutrophil activation protects against the development of chronic pain

@article{Parisien2022AcuteIR,
  title={Acute inflammatory response via neutrophil activation protects against the development of chronic pain},
  author={Marc Parisien and Lucas V. Lima and Concetta Dagostino and Nehme El-Hachem and Gillian L. Drury and Audrey V. Grant and Jonathan Huising and Vivek Verma and Carolina Beraldo Meloto and Jaqueline R. Silva and Gabrielle M.G.S. Dutra and Teodora Markova and Hong Dang and Philippe A. Tessier and Gary D. Slade and Andrea G. Nackley and Nader Ghasemlou and Jeffrey S. Mogil and Massimo Allegri and Luda Diatchenko},
  journal={Science Translational Medicine},
  year={2022},
  volume={14}
}
The transition from acute to chronic pain is critically important but not well understood. Here, we investigated the pathophysiological mechanisms underlying the transition from acute to chronic low back pain (LBP) and performed transcriptome-wide analysis in peripheral immune cells of 98 participants with acute LBP, followed for 3 months. Transcriptomic changes were compared between patients whose LBP was resolved at 3 months with those whose LBP persisted. We found thousands of dynamic… 
Potential Neuroimmune Interaction in Chronic Pain: A Review on Immune Cells in Peripheral and Central Sensitization
TLDR
The mechanisms of regulation of the sensory nervous system by neutrophils, macrophages, mast cells, B cells, T cells, and central glial cells are reviewed to provide new therapeutic ideas and strategies for the control of chronic pain at the immune cellular level.
Neutrophils infiltrate sensory ganglia and mediate chronic widespread pain in fibromyalgia
TLDR
It is shown that neutrophils invade sensory ganglia and confer mechanical hypersensitivity on recipient mice, whilst adoptive transfer of immunoglobulin, serum, lymphocytes or monocytes have no effect on pain behaviour, providing the framework for an immunological basis of chronic widespread pain in fibromyalgia mediated by polymorphonuclear granulocytes.
Neutrophil-Derived COX-2 has a Key Role during Inflammatory Hyperalgesia.
TLDR
It is demonstrated for the first time that neutrophil-derived COX-2 plays a key role in peripheral inflammatory hyperalgesia, and has an important role in the regulation of inflammatory hyperAlgesia.

References

SHOWING 1-10 OF 79 REFERENCES
The transition from acute to chronic pain: understanding how different biological systems interact
TLDR
A better understanding of how chronic pain develops at a mechanistic level can aid clinicians in treating their patients by showing how the underlying biology of chronic pain contributes to the clinical manifestations of pain.
Whole blood transcriptomic profiles can differentiate vulnerability to chronic low back pain
TLDR
The transcriptome of the transition from acute to chronic low back pain was characterized by significant upregulation of antigen presentation pathway (MHC class I and II) genes and downregulation of mitochondrial genes associated with oxidative phosphorylation, suggesting a unique genomic signature of vulnerability to low backPain chronicity.
CD11b+Ly6G− myeloid cells mediate mechanical inflammatory pain hypersensitivity
TLDR
The results show that these two models induced quite different inflammatory processes and that targeted elimination of a subpopulation of nonneutrophil myeloid cells blocked development of mechanical hypersensitivity following incisional wounds, highlighting the significant differences and potential clinical relevance of the incisonal wound model compared with the CFA model.
The Transition of Acute Postoperative Pain to Chronic Pain: An Integrative Overview of Research on Mechanisms.
  • C. Chapman, C. Vierck
  • Medicine
    The journal of pain : official journal of the American Pain Society
  • 2017
Pain regulation by non-neuronal cells and inflammation
TLDR
This work reviews how non-neuronal cells interact with nociceptive neurons by secreting neuroactive signaling molecules that modulate pain and discusses new therapeutic strategies to control neuroinflammation for the prevention and treatment of chronic pain.
Resolution of inflammation: the beginning programs the end
TLDR
Emerging evidence now suggests that an active, coordinated program of resolution initiates in the first few hours after an inflammatory response begins, and the mechanism required for inflammation resolution may underpin the development of drugs that can resolve inflammatory processes in directed and controlled ways.
Neuroinflammation and Central Sensitization in Chronic and Widespread Pain.
TLDR
Neuroinflammation drives widespread chronic pain via central sensitization and sex-dependent glial/immune signaling in chronic pain and new therapeutic approaches that control neuroinflammation for the resolution of chronic pain are discussed.
Acute Low Back Pain: Differential Somatosensory Function and Gene Expression Compared With Healthy No-Pain Controls
TLDR
The acute LBP group exhibited increased pain sensitivity to cold stimuli, mechanical stimuli, including mechanical temporal summation at both the painful back area and remote location suggesting a mechanism of enhanced central nervous system excitability.
When pain gets stuck: the evolution of pain chronification and treatment resistance
TLDR
This review discusses possible contributions and interactions of biological, social, and psychological perturbations that underlie the evolution of treatment-resistant chronic pain and proposes the concept of "stickiness" as a soubriquet for capturing the multiple influences on the persistence of pain and pain behavior.
Variability in the Analgesic Response to Ibuprofen Is Associated With Cyclooxygenase Activation in Inflammatory Pain
TLDR
It is suggested that a less pronounced activation of the inflammatory prostanoid system is associated with insufficient pain relief on ibuprofen alone and the need for additional therapeutic intervention.
...
...