Immuno-Inflammatory Mechanisms in the Chronification of Pain - PubMed

4 days ago

Chronic pain affects 20% of the global population, with current treatments providing meaningful relief in less than 30% of patients.
Immuno-inflammatory mechanisms play a critical role in the transition from acute to chronic pain, involving pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α.
Peripheral tissue injury triggers immune responses, with infiltrating macrophages, T lymphocytes, and mast cells perpetuating pro-nociceptive environments.
Central mechanisms include microglial and astrocytic activation, leading to neuroinflammation, synaptic remodeling, and enhanced excitatory neurotransmission.
The balance between pro-inflammatory (Th1/Th17) and anti-inflammatory (Th2/Treg) immune responses determines pain outcomes.
Premature suppression of acute inflammation with NSAIDs or corticosteroids may disrupt resolution pathways and promote pain chronification.
Local inflammation is more relevant than systemic inflammation for pain persistence.
The gut-brain-immune axis is a novel therapeutic target, with microbiota influencing pain susceptibility through immunomodulation.
Chronic pain represents a failure of natural resolution mechanisms rather than prolonged nociceptive activation.
Future strategies should focus on restoring homeostatic mechanisms and incorporate biomarker-guided, multimodal interventions.

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