BACKGROUND & AIMS: The four principal types of intestinal epithelial cells are derived from multipotent stem cells. Currently, there is no information on factors that regulate commitment of stem cells to differentiate along one lineage vs. another. The aim of our study was to investigate the role of T cells in the regulation of small intestinal goblet cell hyperplasia in mice infected with the parasite Trichinella spiralis. METHODS: NIH mice were infected with T. spiralis, and intestinal goblet cells and cytokine response were studied. Interferon gamma and interleukin 5 were used as candidate T helper (Th)1 and Th2 cytokines, respectively. Adoptive transfer experiments were also performed. RESULTS: Small intestinal goblet cell hyperplasia occurred 8 days after infection with T. spiralis. Th1-type cells were predominant in the mesenteric lymph nodes early in the course of infection, with a switch to Th2-predominant cells around the time of goblet cell hyperplasia. Transfer of Th2-enriched mesenteric lymph node cells further enhanced goblet cell hyperplasia in recipient mice. Neutralization of interleukin 5 activity did not affect T. spiralis-induced goblet cell hyperplasia. CONCLUSIONS: Small intestinal goblet cell hyperplasia in T. spiralis-infected mice is probably regulated by Th2 cells. We postulate that Th2-derived factors (other than interleukin 5) induce stem cells to differentiate preferentially along the goblet cell lineage.
BACKGROUND & AIMS: The four principal types of intestinal epithelial cells are derived from multipotent stem cells. Currently, there is no information on factors that regulate commitment of stem cells to differentiate along one lineage vs. another. The aim of our study was to investigate the role of T cells in the regulation of small intestinal goblet cell hyperplasia in mice infected with the parasite Trichinella spiralis. METHODS: NIH mice were infected with T. spiralis, and intestinal goblet cells and cytokine response were studied. Interferon gamma and interleukin 5 were used as candidate T helper (Th)1 and Th2 cytokines, respectively. Adoptive transfer experiments were also performed. RESULTS: Small intestinal goblet cell hyperplasia occurred 8 days after infection with T. spiralis. Th1-type cells were predominant in the mesenteric lymph nodes early in the course of infection, with a switch to Th2-predominant cells around the time of goblet cell hyperplasia. Transfer of Th2-enriched mesenteric lymph node cells further enhanced goblet cell hyperplasia in recipient mice. Neutralization of interleukin 5 activity did not affect T. spiralis-induced goblet cell hyperplasia. CONCLUSIONS: Small intestinal goblet cell hyperplasia in T. spiralis-infected mice is probably regulated by Th2 cells. We postulate that Th2-derived factors (other than interleukin 5) induce stem cells to differentiate preferentially along the goblet cell lineage.
Authors: Moshe Biton; Avi Levin; Michal Slyper; Irit Alkalay; Elad Horwitz; Hagar Mor; Sharon Kredo-Russo; Tali Avnit-Sagi; Gady Cojocaru; Farid Zreik; Zvi Bentwich; Matthew N Poy; David Artis; Michael D Walker; Eran Hornstein; Eli Pikarsky; Yinon Ben-Neriah Journal: Nat Immunol Date: 2011-01-30 Impact factor: 25.606
Authors: M Gomez-Samblas; J J García-Rodríguez; M Trelis; D Bernal; F J Lopez-Jaramillo; F Santoyo-Gonzalez; S Vilchez; A M Espino; F Bolás-Fernández; A Osuna Journal: Open Biol Date: 2017-04 Impact factor: 6.411
Authors: Riccardo D'Elia; Matthew L DeSchoolmeester; Leo A H Zeef; Steven H Wright; Alan D Pemberton; Kathryn J Else Journal: BMC Genomics Date: 2009-10-24 Impact factor: 3.969