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Quantum and nanoscale sensing of microinflammation for earlier detection of chronic inflammatory and neuroimmune disease
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DOI：10.1186/s11671-026-04830-0.png)
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Abstract
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Chronic inflammatory diseases may begin with spatially restricted and low-abundance inflammatory events that precede overt symptoms. In this perspective, we refer to such early events as micro-inflammation and discuss how mechanistic insights from the IL-6 amplifier and neuroimmune regulation may guide earlier detection of related diseases. The IL-6 amplifier is a positive-feedback inflammatory circuit in non-immune cells driven by concurrent NF-κB and IL-6–STAT3 signaling, whereas the gateway reflex illustrates how defined neural inputs can induce site-specific vascular micro-inflammation and immune-cell entry into affected tissues and organs. We also discuss stress-associated neuroimmune remodeling in diffuse neuropsychiatric systemic lupus erythematosus (dNPSLE) as a representative example of region-specific brain inflammation that may precede overt neuropsychiatric manifestations. On this basis, we examine how quantum and nanoscale sensing platforms, particularly fluorescent nanodiamonds containing nitrogen-vacancy centers and AI-assisted nanopore devices, could be adapted to detect candidate readouts of micro-inflammation, including reactive oxygen species, cytokine-related signals, nucleic acids, and other trace biomarkers. The original contribution of this Perspective is a mechanistically guided framework that maps micro-inflammatory biology related to the IL-6 amplifier, the gateway reflex, and dNPSLE onto specific classes of candidate nanosensing readouts, including oxidative stress-related physicochemical signals, cytokine-associated soluble biomarkers, extracellular nucleic acids, and other trace molecular signatures. Rather than providing a comprehensive review of all inflammatory mechanisms or diagnostic technologies, we present a mechanistically focused perspective linking neuroimmunology to next-generation sensing. We also highlight current limitations, including the predominantly preclinical nature of supporting evidence, uncertainty regarding accessible blood or cerebrospinal fluid biomarkers at presymptomatic stages, and the challenge of translating spatially restricted inflammatory signals into non-invasive human diagnostics.
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