Ginger: New Discoveries on the Effect of Oral Intake in Reducing Neutrophil Hyperactivity in Autoimmune Diseases
Ginger is well-known for its beneficial properties, but recent studies are revealing its potential to attenuate the hyperactivity of immune cells, a common characteristic in certain autoimmune diseases.
Researchers have discovered that 6-gingerol, the most abundant phytochemical in ginger root and the main active compound in ginger, can inhibit phosphodiesterase, thereby reducing excessive neutrophil activity in models of antiphospholipid syndrome (APS) and lupus.
This study explored the extent to which oral intake of a whole ginger extract would similarly influence neutrophils in both autoimmune mice and healthy humans.
In vitro, a solubilized ginger extract was able to attenuate the formation of neutrophil extracellular traps (NETosis) by human neutrophils through a mechanism dependent on cyclic AMP-dependent kinase, protein kinase A.
When mice with characteristics of antiphospholipid syndrome or lupus were treated orally with a ginger extract, they showed a reduction in circulating NETs, as well as the moderation of other disease outcomes such as large vein thrombosis (APS) and autoantibody production (lupus).
In a pilot clinical trial, validated in a second cohort, daily intake of a ginger supplement for 7 days by healthy volunteers increased cAMP levels in neutrophils, inhibited NETosis in response to disease-relevant stimuli, and reduced levels of circulating plasma NETs.
In summary, this work demonstrates that ginger intake limits immune cell hyperactivity in autoimmune mouse models and that ginger consumption by healthy individuals makes these cells more resistant to extracellular trap formation.
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Source: Ali RA, Minarchick VC, Zahavi M, Rysenga CE, Sturm KA, Hoy CK, Sarosh C, Knight JS, Demoruelle MK. Ginger intake suppresses neutrophil extracellular trap formation in autoimmune mice and healthy humans. JCI Insight. 2023 Sep 22;8(18):e172011. doi: 10.1172/jci.insight.172011. PMID: 37737262; PMCID: PMC10561719.
