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Isolation and Flow Cytometric Characterization of Murine Small Intestinal Lymphocytes
Published on: May 8, 2016
Soybean-Derived Soluble Fiber Enhances Antimicrobial Proteins in the Mouse Small Intestine via a Tuft Cell-Group 2
Arslan Ahmad1, Bambang Dwi Wijatniko1,2, Cláudia Domingos Mapure Siueia1
1Graduate School of Integrated Sciences for Life, Hiroshima University, 1-4-4 Kagamiyama, Higashi-Hiroshima 739-8528, Japan.
Abstract:
Water-soluble soybean fiber (WSSF) exerts health benefits beyond its fermentability, but its direct effects on epithelial-immune interactions remain unclear. We investigated whether WSSF regulates antimicrobial proteins (AMPs) in the small intestine and the underlying mechanisms. C57BL/6J and tuft cell-deficient Pou2f3-knockout mice were fed control or WSSF-supplemented diets, and gene and protein expression and cecal microbiota were analyzed. WSSF upregulated the epithelial AMPs SPRR2A, RELMβ, and ANG4 in the jejunum and ileum. Pharmacological inhibition of group 2 innate lymphoid cells (ILC2) or TRPM5 attenuated AMP induction and reduced IL-25, IL-13, tuft cell markers, and STAT6 phosphorylation. WSSF also failed to induce AMPs or type 2 immune markers in Pou2f3-knockout mice, indicating a requirement for tuft cells. Finally, WSSF altered cecal microbiota composition in a tuft cell-dependent manner. These findings identify WSSF as a soybean-derived fiber that strengthens epithelial innate defense via a TRPM5-tuft cell-ILC2 axis.
Insights
Water-soluble soybean fiber (WSSF) enhances gut immunity by boosting antimicrobial proteins (AMPs) in the small intestine. This effect relies on TRPM5 channels, tuft cells, and group 2 innate lymphoid cells (ILC2s).
Area of Science:
- Gastroenterology
- Immunology
- Microbiology
Background:
- Water-soluble soybean fiber (WSSF) offers health benefits beyond fermentation.
- Its precise impact on epithelial-immune cell communication is not fully understood.
Purpose of the Study:
- To investigate WSSF's role in regulating small intestinal antimicrobial proteins (AMPs).
- To elucidate the underlying molecular and cellular mechanisms involved.
Main Methods:
- Utilized C57BL/6J and tuft cell-deficient Pou2f3-knockout mice fed control or WSSF diets.
- Analyzed gene/protein expression, immune cell markers, and cecal microbiota composition.
- Employed pharmacological inhibition of TRPM5 channels and group 2 innate lymphoid cells (ILC2s).
Main Results:
- WSSF upregulated jejunal and ileal AMPs (SPRR2A, RELMβ, ANG4).
- ILC2 inhibition or TRPM5 blockade reduced AMP induction, IL-25, IL-13, and tuft cell markers.
- AMP induction and type 2 immunity markers were absent in Pou2f3-knockout mice.
- WSSF modulated cecal microbiota composition in a tuft cell-dependent manner.
Conclusions:
- WSSF strengthens intestinal innate defense by upregulating epithelial AMPs.
- This process involves a signaling axis comprising TRPM5, tuft cells, and ILC2s.
- WSSF modulates the gut microbiota through a tuft cell-dependent pathway.

