CFTR High Expresser Cells in cystic fibrosis and intestinal diseases
Diego Carlos dos Reis,
Parinaz Dastoor,
Anderson Kenedy Santos,
Kaelyn Sumigray,
Nadia A. Ameen
Affiliations
Diego Carlos dos Reis
Department of Pediatrics/Gastroenterology and Hepatology, Yale School of Medicine, CT, 06510, USA
Parinaz Dastoor
Department of Pediatrics/Gastroenterology and Hepatology, Yale School of Medicine, CT, 06510, USA
Anderson Kenedy Santos
Department of Pediatrics/Gastroenterology and Hepatology, Yale School of Medicine, CT, 06510, USA; Department of Genetics, Yale School of Medicine, New Haven, CT, 06510, USA
Kaelyn Sumigray
Department of Genetics, Yale School of Medicine, New Haven, CT, 06510, USA; Yale Stem Cell Center, Yale School of Medicine, New Haven, CT, 06510, USA; Yale Cancer Center, Yale School of Medicine, New Haven, CT, 06510, USA
Nadia A. Ameen
Department of Pediatrics/Gastroenterology and Hepatology, Yale School of Medicine, CT, 06510, USA; Department of Cellular and Molecular Physiology, Yale School of Medicine, New Haven, CT06510, USA; Corresponding author. Department of Pediatrics/Gastroenterology and Hepatology, Yale School of Medicine, CT, 06510, USA.
Cystic Fibrosis Transmembrane Conductance Regulator (CFTR), the Cl−/HCO3− channel implicated in Cystic Fibrosis, is critical to the pathophysiology of many gastrointestinal diseases. Defects in CFTR lead to intestinal dysfunction, malabsorption, obstruction, infection, inflammation, and cancer that increases morbidity and reduces quality of life. This review will focus on CFTR in the intestine and the implications of the subpopulation of CFTR High Expresser Cells (CHEs) in Cystic Fibrosis (CF), intestinal physiology and pathophysiology of intestinal diseases.
