Gut bacteria chemicals can help control certain immune cells involved in asthma by changing how their genes are expressed.
Scientific Claim
SCFAs may regulate ILC2 proliferation in allergic asthma through HDAC inhibition.
Source Excerpt
“Systemic and local administration of C4 attenuates ILC2-driven airway hyperresponsiveness and eosinophil inflammation. C4 can regulate the expression of ILC2s and inhibit their proliferation at the transcriptional level. C4 inhibits the proliferation of ILC2s and the production of the cytokines IL-5 and IL-13 by inhibiting the activity of HDAC without affecting cell viability and without being mediated by the activation of GPR41 or GPR43.”
Evidence from Studies
Supporting Studies
Regulation of short-chain fatty acids in the immune system
The study describes how SCFAs may regulate ILC2 proliferation in allergic asthma through HDAC inhibition. This is a descriptive claim about observed mechanisms in the literature.
⚠️ Overstated
The study uses definitive language ('attenuates', 'inhibit', 'inhibits') but is a review summarizing existing research. It cannot establish definitive causal relationships between SCFAs and ILC2 proliferation.
More accurate phrasing:
“SCFAs may be associated with regulation of ILC2 proliferation in allergic asthma through HDAC inhibition.”