Biologyarticle2026-08-11

Recovery-Primed Stimulation: A Proposed Framework for Controlled Triggering of Healing-Related Physiology in Low-Grade Chronic Inflammation

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Abstract

Low-grade chronic inflammation (LGCI) is considered a heterogeneous, persistent, high-burden biological state rather than a single disease entity. In LGCI, inflammation-related pathways can reinforce each other, creating a self-sustaining inflammatory state. This creates a treatment-design problem: stimulation delivered into LGCI biology that is already primed by persistent inflammatory drivers and has not fully returned to a resolved resting state may produce the expected, wanted biological effects, such as braking, resolution, repair, or regulatory recovery, but may also worsen LGCI by adding inflammatory drive to already active inflammatory pathway loops. This unwanted effect may include nuclear factor kappa B (NF-κB) or inflammasome reactivation, cytokine-loop amplification, flare response, increased autonomic-inflammatory pressure, temporal summation, or adverse carryover. Recovery-primed stimulation (RP) is a proposed framework for controlled triggering of healing-related physiology followed by recovery-compatible repetition. In RP, a biochemical, biophysical, or combined input is used as a controlled trigger of wanted healing-related physiology, and repetition is delayed until the induced wanted response has had time to unfold and unwanted carryover is absent or acceptable. The hypothesis is that RP may better fit LGCI physiology than dense repetition and may improve the balance between wanted and unwanted effects. RP extends this controlled-triggering and recovery-compatible-repetition logic across biochemical, biophysical, or combined inputs and across multiple LGCI-relevant target pathway axes. It is presented as an interdisciplinary technology platform for controlled biological triggering in low-threshold, slow-recovery biology.

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Authors: Wilfried Van Moorleghem, Mark Mikhail, Peter Besselink, Luis Chin, Alejandra Velazquez, Melia Matuz Velasquez, Diego A Montelongo Mercado