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The increase in nitric oxide is particularly intriguing since alpha-1 antitrypsin has been shown to inhibit iNOS, nitric oxide release and NF-kB activation, suggesting that alpha-1 antitrypsin replacement therapy or other neutrophil elastase inhibitor therapies may help decrease oxidative stress and inflammation

Moreover, metabolic flux analysisusing isotope tracing and computational modelingcan quantify substrate utilization and biosynthetic pathway engagement, providing mechanistic insights into metabolic bottlenecks that limit immune cell fitness or support cancer stem-like cells stemness

doi: 10.1038/nature25486