Gut bacteria chemicals can help guide white blood cells called neutrophils to infection sites by activating specific receptors and signaling pathways.
Scientific Claim
SCFAs may regulate neutrophil recruitment to inflammatory sites through GPR43 receptor activation and intracellular protein kinase P38 signaling.
Source Excerpt
“SCFAs increase the expression of L-selectin on the surface of neutrophil granulocytes, activate neutrophil chemotactic recruitment to the inflammatory site, and aggravate the inflammatory process without affecting the expression of β2 integrin mRNA. SCFAs induce the aggregation of neutrophils to the site of inflammation through the CPR43 receptor. This process is associated with the activation of intracellular protein kinase P38 and the coupling of Gi/o and Gq proteins.”
Evidence from Studies
Supporting Studies
Regulation of short-chain fatty acids in the immune system
The study describes mechanisms by which SCFAs may influence neutrophil recruitment through GPR43 receptor activation and P38 signaling. This is a descriptive claim about observed mechanisms in the literature.
⚠️ Overstated
The study uses definitive language ('increase', 'activate', 'induce') but is a review summarizing existing research. It cannot establish definitive causal relationships between SCFAs and neutrophil recruitment.
More accurate phrasing:
“SCFAs may be associated with neutrophil recruitment to inflammatory sites through GPR43 receptor activation and intracellular protein kinase P38 signaling.”