Gastric tuft cells express DCLK1 and are expanded in hyperplasia

Milena Saqui-Salces, Theresa M. Keeley, Ann S. Grosse, Xiaotan T. Qiao, Mohamad El-Zaatari, Deborah L. Gumucio, Linda C. Samuelson, Juanita L. Merchant

Research output: Contribution to journalArticlepeer-review

59 Scopus citations

Abstract

Epithelial tuft cells are named after their characteristic microtubule bundles located at the cell apex where these are exposed to the luminal environment. As such, tuft cells are found in multiple organs, including the gastrointestinal (GI) tract where the apical "tuft" is hypothesized to detect and transmit environmental signals. Thus, the goal of our study was to characterize gastric tuft cells during GI tract development, then subsequently in the normal and metaplastic adult stomach. GI tracts from mouse embryos, and newborn and postnatal mice were analyzed. Tuft cells were identified by immunohistochemistry using acetylated-α-tubulin (acTub) antibody to detect the microtubule bundle. Additional tuft cell markers, e.g., doublecortin-like kinase 1 (DCLK1), were used to co-localize with acTub. Tuft cells were quantified in human gastric tissue arrays and in mouse stomachs with or without inflammation. In the developing intestine, tuft cells in both the crypts and villi expressed all markers by E18.5. In the stomach, acTub co-localized with DCLK1 and other established tuft cell markers by E18.5 in the antrum, but not until postnatal day 7 in the corpus, with the highest density of tuft cells clustered at the forestomach ridge. Tuft cell numbers increased in hyperplastic human and mouse stomachs. In the adult GI tract, the tuft cell marker acTub co-expressed with DCKL1 and chemosensory markers, e.g.,TRPM5. In summary, tuft cells appear in the gastric antrum and intestine at E18.5, but their maximal numbers in the corpus are not achieved until after weaning. Tuft cell numbers increase with inflammation, hyperplasia, and metaplasia.

Original languageEnglish (US)
Pages (from-to)191-204
Number of pages14
JournalHistochemistry and Cell Biology
Volume136
Issue number2
DOIs
StatePublished - Aug 2011

Bibliographical note

Funding Information:
Acknowledgments This study was supported by NIH Grant P01-DK62041 (J.L.M.), NIH Grants RO1-DK078926 (L.C.S.), and University of Michigan Digestive Disease Center Grant P30-DK-34933.

Keywords

  • Brush cells
  • Chemosensory
  • Development
  • Metaplasia
  • Stomach
  • TRPM5

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