Gut bacteria chemicals can help reduce allergic lung inflammation by making certain white blood cells die off and reducing their movement to the lungs.
Scientific Claim
SCFAs may reduce eosinophil infiltration in allergic airway inflammation through HDAC inhibition and apoptosis induction.
Source Excerpt
“In a mouse model of allergic airway inflammation, a high-fiber diet, probiotics, or direct administration of SCFAs effectively reduced airway eosinophils by altering the gut microbiome and SCFA levels. Similarly, SCFAs exert the same effect in eosinophilia-related diseases (including asthma, atopic dermatitis, inflammatory bowel diseases, and eosinophilic oesophagitis). A recent study illustrated the mechanism through which SCFAs directly affect eosinophils. Eosinophils treated with C3 and C4 exhibit decreased cell size and number, loss of bilobate nuclei, mitochondrial membrane potential depolarization, and effector caspase activation, which results in the induction of apoptosis by regulating intracellular pathways, a process that may be mediated by inhibition of HDAC independent of the GPR41 and GPR43 receptor pathways.”
Evidence from Studies
Supporting Studies
Regulation of short-chain fatty acids in the immune system
The study describes how SCFAs may reduce eosinophil infiltration in allergic airway inflammation through HDAC inhibition and apoptosis induction. This is a descriptive claim about observed mechanisms in the literature.
⚠️ Overstated
The study uses definitive language ('reduced', 'exert the same effect', 'results in the induction of apoptosis') but is a review summarizing existing research. It cannot establish definitive causal relationships between SCFAs and reduced eosinophil infiltration.
More accurate phrasing:
“SCFAs may be associated with reduced eosinophil infiltration in allergic airway inflammation through HDAC inhibition and apoptosis induction.”