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Intestinal Peyer’s patches prevent tumorigenesis in Apc(Min/+) mice

Peyer’s patches are nodules that play a central role in intestinal immunity. Few studies demonstrate the relationship between the number of Peyer’s patches and intestinal polyps. Here we identify a statistically significant inverse correlation between the quantity of Peyer’s patches and of the devel...

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Detalles Bibliográficos
Autores principales: Fujimoto, Kyoko, Fujii, Gen, Sakurai, Hitomi, Yoshitome, Hiroko, Mutoh, Michihiro, Wada, Morimasa
Formato: Online Artículo Texto
Lenguaje:English
Publicado: the Society for Free Radical Research Japan 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4306656/
https://www.ncbi.nlm.nih.gov/pubmed/25678750
http://dx.doi.org/10.3164/jcbn.14-115
Descripción
Sumario:Peyer’s patches are nodules that play a central role in intestinal immunity. Few studies demonstrate the relationship between the number of Peyer’s patches and intestinal polyps. Here we identify a statistically significant inverse correlation between the quantity of Peyer’s patches and of the development of intestinal polyps in Apc(Min/+) mice, which are a useful model to clarify the role of Peyer’s patches in intestinal tumorigenesis. Using this model, we increased the number of Peyer’s patches using 0.1% and 1% corn husk arabinoxylan through feed. Intestinal polyp formation significantly decreased, concomitant with an increase in Peyer’s patches development (n = 12/group). In Aly(−/−)Apc(Min/+) mice (negative control; no Peyer’s patches) there was no change in the amount of intestinal polyps (n = 10/group). Immune reaction following corn husk arabinoxylan treatment was measured by cytokine array. Increasing the number of Peyer’s patches decreased interleukin-17 production, which showed a dose dependent correlation with transcription factor/lymphoid enhancer-binding factor. This study identified a relationship between levels of Peyer’s patches and intestinal polyp formation, partly explained by the involvement of interleukin-17 production and β-catenin signaling in Apc(Min/+) mice.