Impact of oral administration of compost extract on gene expression in the rat gastrointestinal tract
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Updated: May 20, 2026

Effects of Taste Signaling Protein Abolishment on Gut Inflammation in an Inflammatory Bowel Disease Mouse Model
Published on: November 9, 2018
Takashi Satoh1, Takumi Nishiuchi, Tomoaki Naito
1Division of Molecular Hematology, Kitasato University Graduate School of Medical Sciences, 1-15-1 Kitasato, Minami-ku, Sagamihara 252-0373, Japan.
Abstract:
Oral administration of an extract consisting of compost fermented with thermophiles to pigs reduces the incidence of stillbirth and promotes piglet growth. However, the mechanism by which the compost extract modulates the physiological conditions of the animals remains largely unknown. Here, we investigate the effects of compost extract on the physiological responses in the intestine of a mammalian rat model. The level of fecal immunoglobulin A (IgA), which provides protection against pathogens and is secreted from the small intestine, was significantly higher in rats treated with continuous administration of the compost extract than in untreated rats after 2 months, but not after 1 month. However, the fecal IgA level was not significantly different in rats that received the filtered compost extract compared with the untreated rats or the rats that received the compost extract. Gene expression analyses of the small intestine indicated that several immune-related genes were upregulated following compost exposure. Specifically, the expression levels of lymphocyte chemoattractant chemokine CXCL13 and Granzyme B, which is released within cytotoxic T lymphocytes and natural killer cells, increased in the small intestinal tract following compost exposure. Based on these observations, it was postulated that the increased level of fecal IgA following compost exposure was associated with the expression of CXCL13 and Granzyme B in the intestinal tract. Thus, thermophile-fermented compost could contain microbes or substances that activate the rat's gut mucosal immune response.

