Inflammation &
Immune Signaling
Chronic, low-grade inflammation — often called "inflammaging" — is one of the biological signatures researchers track across the lifespan (PMID 30046148). Transcriptomics reads inflammatory cytokine and resolution genes at the point where they are switched on: transcription.
Reading Inflammation at the Transcript Level
Circulating proteins like C-Reactive Protein (CRP) are commonly used to track inflammation, but a single CRP value carries substantial within-person variability and no information about which tissue the signal came from.
Inflammation transcriptomics measures active gene transcription. Tracking NF-κB, IL6, and anti-inflammatory genes such as IL10 describes which inflammatory and resolution programs are transcriptionally active at the time of the sample.
Transcription is upstream of the circulating proteins a blood panel measures, so a transcriptional panel and a protein panel describe different layers of the same biology.
Key Pathway Targets
Nuclear Factor kappa B Subunits 1 and 2
Primary transcriptional orchestrator of inflammatory cytokine cascades.
Interleukin 6
Key pro-inflammatory cytokine linked to acute and chronic systemic inflammation.
Tumor Necrosis Factor (TNF-α)
Potent inflammatory signaling cytokine implicated in tissue catabolism.
Interleukin 10
Crucial anti-inflammatory cytokine that inhibits transcription of pro-inflammatory factors.
Transforming Growth Factor Beta 1
Pleiotropic regulator of immune tolerance and tissue remodeling; context determines whether its effect is resolving or fibrotic.
Why DNA Tells Only Half the Inflammatory Story
Your static DNA codes for variants in inflammatory cytokines, such as promoter SNPs in the TNF-α gene. These variations describe inherited tendencies in how inflammatory genes are regulated. They do not change over your lifetime, and they say nothing about what those genes are doing right now.
Transcriptomics (RNA) measures cytokine transcription as it is happening. Because transcription responds to conditions rather than inheritance, a transcriptional panel reflects the state of those genes at the moment the sample was taken — not a fixed trait.
Protein Panels vs. Transcriptomics
Traditional inflammation panels measure proteins circulating in the bloodstream. Transcriptomics measures the gene transcription upstream of them. The two describe different layers of the same biology; the table below pairs each protein marker with the transcripts that sit upstream of it.
| Protein Marker | What It Measures | RNA Target |
|---|---|---|
| hs-CRP | Liver-derived acute-phase protein; responds within hours but carries no information about tissue source. | NFKB1 |
| Erythrocyte Sed Rate (ESR) | Reflects fibrinogen and immunoglobulin levels; rises and falls over days rather than hours. | IL6 / TNF |
| Serum Cytokines | Present at very low concentrations, and the value returned depends heavily on the assay used. | IL10 / TGFB1 |
WHAT A TRANSCRIPTIONAL PANEL DOES NOT TELL YOU
- × That you have, or do not have, any medical condition. This panel reports gene activity, not diagnoses.
- × Whether a therapy is working. Transcript levels move for many reasons — sleep, a recent infection, the time of day, how long since you last ate or trained — and a change in them is not evidence that any intervention succeeded or failed.
- × What your results will be next month. Every value describes the moment the sample was drawn. Single-timepoint transcript measurements carry substantial within-person variability.
- × What is happening in a tissue the sample did not come from. These panels run on a blood sample. A blood transcript level is not a muscle, liver, brain or adipose measurement.
The NF-κB Activation and Resolution Cascade
Inflammation is regulated by a switch. When tissues experience stress, pattern-recognition and cytokine receptors activate the transcription factor NF-κB, which moves to the nucleus and drives transcription of primary cytokines. Resolution requires a separate set of counter-regulatory genes (PMID 29158945).
Stress Stimulus
Pathogens, toxins, or tissue injury are sensed by Toll-like receptors and by the IL-1 and TNF receptors.
NF-κB Translocation
IKK phosphorylates IκB, marking it for degradation and freeing NF-κB (NFKB1) to enter the nucleus.
Cytokine Transcription
Upregulated mRNA of TNF and IL6 initiates localized immune cell recruitment.
Immune Resolution
IL10 signals back through its own receptor via JAK1 and STAT3, repressing further pro-inflammatory transcription (PMID 30995504).
Three Health Domains. Deliberately No Composite Score.
Standard tests reduce inflammation to an isolated protein like hs-CRP. Inflammation Compass profiles the circulating leukocyte transcriptome and organizes gene activity into three separately scored Health Domains against a healthy adult reference cohort.
Activation
Quantifies the engagement of primary inflammatory machinery: danger sensing, IL-1 signaling, neutrophil and monocyte deployment, and platelet containment across 7 biological pathways.
Antiviral Response
Measures the coordinated type I interferon program (4 transcriptional modules evaluated as 1 grouped pathway). Usually sits low in healthy individuals and rises with viral exposure or vaccination.
Resolution
Reads the active counter-regulatory programs that stand down and terminate the inflammatory cascade across 2 pathways. Standard tests like hs-CRP are entirely blind to this recovery phase.
The Clinical Rationale: Why There Is Deliberately No Aggregate Score
Core Architectural RuleCollapsing three independent biological programs into a single composite index would conceal the exact pattern the test exists to reveal: whether an inflammatory response is proportionate and whether it is being closed out.
Elevated Activation accompanied by robustly elevated Resolution reflects a healthy immune system managing an acute perturbation (a hard workout, a recent vaccination, or a transient cold) that is actively standing down.
Elevated Activation with Resolution flat or suppressed is the clinical pattern that warrants attention: inflammatory machinery is firing without the counter-regulatory brake engaged.
An arbitrary single "inflammation score" would average these two opposite physiological states into identical numbers. Reporting each domain independently ensures complete biological clarity for clinician interpretation.
Within-Sample Rank Normalization
Modules are drawn from the established blood transcriptional module repertoire (Chaussabel and colleagues) and confirmed across ~2,500 whole-blood transcriptomes. Each module is scored within-sample as the mean percentile rank of its genes. Because each sample serves as its own reference, scores are stable against sequencing batch variation and ideally calibrated for longitudinal tracking across baseline, 1-month, 3-month, and annual evaluations.
Inputs That Affect Inflammatory Signaling
Each of these has published evidence bearing on inflammatory signaling. The strength of that evidence differs considerably between them, and is noted on each card.
EPA & DHA Omega-3 Fatty Acids
EPA and DHA are the substrate precursors for resolvins and protectins, specialized pro-resolving mediators that actively terminate the inflammatory response rather than suppressing it (PMID 29757195).
Bioactive Curcumin
Dietary supplementInterferes with IκB kinase signaling in cell and animal models. Its oral bioavailability in humans is poor — low absorption, rapid metabolism, rapid elimination — which is the main limit on translating those findings (PMID 17999464).
Sleep
In a meta-analysis of 72 studies (n > 50,000), sleep disturbance was associated with higher CRP and IL-6. The same analysis found no association for experimental short-term sleep deprivation, so the signal tracks sustained disturbance rather than a single bad night (PMID 26140821).
Vagus Nerve Stimulation (ACh Pathway)
Engages the cholinergic anti-inflammatory pathway, in which vagal acetylcholine signaling suppresses macrophage cytokine production (PMID 17273548). This is a device-based intervention, not a lifestyle change.
Therapies That Act on These Pathways
These therapies act on genes this panel reports. Biomeme does not prescribe, supply, recommend or evaluate any of them, and listing one here is not a claim that it works. Several are available only by prescription; some are not approved for any use. Where the published evidence is thin or points the other way, the card says so.
KPV
Not approved for any useInhibits NF-κB activation in human cell lines and reduces inflammation in rodent models (PMID 18061177). There are no published human studies of KPV.
HRT
Prescription onlyRoute matters and the direction is not what most people assume: pooling 107 randomized trials, oral hormone therapy raised CRP by 37.6% (95% CI 17.4–61.3%), while transdermal preparations had no effect on it (PMID 16918589).
GLP-1 receptor agonists
Prescription onlyIn a meta-analysis of 52 randomized trials in type 2 diabetes, GLP-1 receptor agonists lowered CRP (SMD −0.63, 95% CI −1.03 to −0.23). The IL-6 result is inconsistent across meta-analyses of the same trial base (PMID 40230207). These are circulating protein measurements, not transcriptional ones.
Scientific Citations (10)
- [1] Franceschi C, Garagnani P, Parini P, Giuliani C, Santoro A. Inflammaging: a new immune-metabolic viewpoint for age-related diseases. Nat Rev Endocrinol. 2018;14(10):576-590.
- [2] Liu T, Zhang L, Joo D, Sun SC. NF-κB signaling in inflammation. Signal Transduct Target Ther. 2017;2:17023.
- [3] Ouyang W, O'Garra A. IL-10 Family Cytokines IL-10 and IL-22: from Basic Science to Clinical Translation. Immunity. 2019;50(4):871-891.
- [4] Serhan CN, Levy BD. Resolvins in inflammation: emergence of the pro-resolving superfamily of mediators. J Clin Invest. 2018;128(7):2657-2669.
- [5] Anand P, Kunnumakkara AB, Newman RA, Aggarwal BB. Bioavailability of curcumin: problems and promises. Mol Pharm. 2007;4(6):807-818.
- [6] Irwin MR, Olmstead R, Carroll JE. Sleep Disturbance, Sleep Duration, and Inflammation: A Systematic Review and Meta-Analysis of Cohort Studies and Experimental Sleep Deprivation. Biol Psychiatry. 2016;80(1):40-52.
- [7] Tracey KJ. Physiology and immunology of the cholinergic antiinflammatory pathway. J Clin Invest. 2007;117(2):289-296.
- [8] Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, Yan Y, Sitaraman S, Merlin D. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008;134(1):166-178.
- [9] Salpeter SR, Walsh JM, Ormiston TM, Greyber E, Buckley NS, Salpeter EE. Meta-analysis: effect of hormone-replacement therapy on components of the metabolic syndrome in postmenopausal women. Diabetes Obes Metab. 2006;8(5):538-554.
- [10] Ren Y, Chen Y, Zheng W, et al. The effect of GLP-1 receptor agonists on circulating inflammatory markers in type 2 diabetes patients: A systematic review and meta-analysis. Diabetes Obes Metab. 2025;27(7):3607-3626.
The Biomeme Molecular Ecosystem
From deep whole-transcriptome sequencing in the laboratory to rapid point-of-care instrumentation in the field.
High-Depth RNA Sequencing
Processed at One Health Labs, Biomeme's CLIA-certified laboratory, using Illumina NovaSeq high-depth paired-end RNA sequencing. Samples are collected in venous PAXgene blood RNA tubes to stabilize cellular transcription at the moment of draw.
Biomeme/5 Handheld Platform
Beyond central-lab genomics, Biomeme engineers patented, battery-powered real-time PCR instruments. Our deployable hardware brings decentralized molecular detection directly to the field and clinical points of care.
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ABOUT THESE PANELS
Biomeme's wellness transcriptomic panels are general wellness products. They report gene activity to support a healthy lifestyle. They are not intended to diagnose, treat, cure, mitigate or prevent any disease or condition, and they are not a substitute for evaluation by a licensed healthcare professional. Results describe the state of the measured transcripts at the moment the sample was taken.