What is behind Lung & Respiratory
Airway reactivity â the type-2 inflammatory response behind allergic breathing. A possible sign reversal: the same immune slant may increase resistance to some viruses while worsening allergy. Evidence B — Preclinical.
A master inflammatory messenger of the immune system.
Chronic low-grade inflammation in peripheral tissue — vessel wall, myocardium, follicle, joint. Evidence B — Preclinical.
A cytokine with two faces. Chronically elevated it is a core inflammaging marker; acutely released from contracting muscle it is a myokine with metabolic benefit. Same molecule, opposite meaning by context. Evidence B — Preclinical.
The master inflammatory switch — indispensable to defend against threat, corrosive when it never stands down. Evidence B — Preclinical.
The transcription factor that commands the body's own antioxidant and detoxification arsenal. Evidence A — Human trial evidence.
Ventilatory capacity — how much air moves and how fast. A null the evidence keeps: in reflux-related airway complaints, FEV1, fvc and pef did not move; only peripheral oscillometric resistance did. Evidence A — Human trial evidence.
Evidence on these pathways
IL-6 → Systemic Inflammation. “IL-6 is the chief stimulator of the production of most acute phase proteins [8], whereas the other implicated cytokines influence subgroups of acute phase proteins.” — Interleukin-6 and chronic inflammation. Arthritis Research & Therapy, 2006, volume 8, Suppl 2, S3. doi:10.1186/ar1917
NF-κB → CD38 NADase. “Regulation of CD38 expression in HASM cells involves the transcription factor NF-κB, and glucocorticoids inhibit this expression through NF-κB-dependent and -independent mechanisms.” — Regulation of the cd38 promoter in human airway smooth muscle cells by TNF-α and dexamethasone. Respiratory Research, 2008, vol 9, 26. doi:10.1186/1465-9921-9-26
NF-κB → COX-2 Induction. “Moreover, the nuclear factor kappa B (NF-κB) inhibitor BAY11‐7085 or the TLR4 neutralizing antibody markedly blocked PM2.5-induced IL-6 and COX-2 expression.” — PM2.5 exposure upregulates pro-inflammatory protein expression in human microglial cells via oxidant stress and TLR4/NF-κB pathway. Ecotoxicology and Environmental Safety, 2024, vol 277, article 116386. doi:10.1016/j.ecoenv.2024.116386
NF-κB → Kynurenine Pathway. “Treatment of vaccinated DCs with pharmacological NF-κB inhibitors ACHP or DHMEQ significantly inhibited IDO1 biosynthesis, suggesting a role for NF-κB signaling in vaccine up-regulation of dendritic cell IDO1.” — Induction of Indoleamine 2, 3-Dioxygenase in Human Dendritic Cells by a Cholera Toxin B Subunit—Proinsulin Vaccine. PLoS ONE, 2015, volume 10, e0118562. doi:10.1371/journal.pone.0118562
Formulas that act on these pathways
Acts on 5 of these pathways: Airway Reactivity, Systemic Inflammation, NF-κB, Nrf2, Lung Function.
Acts on 4 of these pathways: Systemic Inflammation, IL-6, NF-κB, Nrf2.
Acts on 4 of these pathways: Systemic Inflammation, IL-6, NF-κB, Nrf2.
Acts on 4 of these pathways: Systemic Inflammation, IL-6, NF-κB, Nrf2.
Acts on 4 of these pathways: Systemic Inflammation, IL-6, NF-κB, Nrf2.
Acts on 4 of these pathways: Systemic Inflammation, IL-6, NF-κB, Nrf2.
What this page does not claim
This page names the pathways involved and the published evidence on each. It does not claim that any formula treats, cures or prevents Lung & Respiratory. A pathway opens here only on graded, published evidence, under a standard fixed before the evidence was gathered, and every figure above carries its grade.
These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease.