Neonatal Gut Microbiota Propionate Suppresses Later Airway Inflammation via GPR41 (Hiroshi Ohno)
The human body carries about 40 trillion bacteria, mostly in the colon, and NGS/16S sequencing shows their composition differs in asthma and other immune and metabolic diseases. Using multi-omics spanning genomes, transcriptomes, proteins and metabolites, the team found that propionate from gut microbiota in the neonatal window is received by GPR41-high cells (ILC2/eosinophil-associated) in the small intestinal lamina propria and lung, upregulating genes such as kindlin and suppressing later airway inflammation. The propionate-GPR41 axis sets a protective imprint mainly in the neonatal period, with effects emerging later in life (after about age 5 in humans), suggesting early microbiota intervention may be a time window for asthma prevention. The video is a lecture excerpt; final mechanistic details should be checked against the original paper.
Background: The human body hosts roughly 40 trillion bacteria (mainly in the large intestine); NGS/16S sequencing has revealed that the microbiota composition in immune and metabolic diseases such as asthma differs from healthy controls, and this team focuses on allergy, especially asthma. ; Methodology: A multi-omics strategy of 'genome + transcriptome + proteome + metabolome' is used, rather than only looking at gene catalogs, to dissect how the microbiota affects the host. ; Key mechanism: During the neonatal window, propionate signals produced by the gut microbiota are received by GPR41-high cells (ILC2/eosinophil-associated populations) in the small intestinal lamina propria and lung tissue, upregulating genes such as kindlin, thereby suppressing later airway inflammation. ; Translational implication: The propionate–GPR41 axis mainly establishes its protective imprint during the 'neonatal window,' with effects emerging later in life (after about age 5 in humans), suggesting that early microbiota intervention may be a time window for asthma prevention. ; Limitations: The video is a lecture excerpt; the definitive mechanisms for specific cell types and signaling pathways should be verified against the original papers (the transcript is auto-generated captions, and some terms are phonetic approximations).
- Background: The human body hosts roughly 40 trillion bacteria (mainly in the large intestine); NGS/16S sequencing has revealed that the microbiota composition in immune and metabolic diseases such as asthma differs from healthy controls, and this team focuses on allergy, especially asthma.
- Methodology: A multi-omics strategy of 'genome + transcriptome + proteome + metabolome' is used, rather than only looking at gene catalogs, to dissect how the microbiota affects the host.
- Key mechanism: During the neonatal window, propionate signals produced by the gut microbiota are received by GPR41-high cells (ILC2/eosinophil-associated populations) in the small intestinal lamina propria and lung tissue, upregulating genes such as kindlin, thereby suppressing later airway inflammation.
- Translational implication: The propionate–GPR41 axis mainly establishes its protective imprint during the 'neonatal window,' with effects emerging later in life (after about age 5 in humans), suggesting that early microbiota intervention may be a time window for asthma prevention.
- Limitations: The video is a lecture excerpt; the definitive mechanisms for specific cell types and signaling pathways should be verified against the original papers (the transcript is auto-generated captions, and some terms are phonetic approximations).
Source: YouTube