Direct evidence of mast cell participation in acute acid-induced esophageal inflammation in mice

Jeffrey A. Morganstern, Ming Yu Wang, Barry K. Wershil*

*Corresponding author for this work

Research output: Contribution to journalArticle

6 Scopus citations

Abstract

OBJECTIVES: Mast cells have been implicated in the pathogenesis of esophagitis resulting from gastroesophageal acid reflux, but their precise role has been difficult to define. We proposed to directly examine the contribution of mast cells to neutrophil infiltration in a mouse model of acid-induced esophageal injury. MATERIALS AND METHODS: Normal and mast cell-deficient (Kit) mice underwent either a surgical procedure to induce acute acid reflux injury of the esophagus or sham surgery. Neutrophil infiltration in the esophagus was determined by morphometrical quantification. To further delineate the involvement of mast cells, acid-induced esophageal injury was elicited in mast cell-deficient mice that had undergone mast cell reconstitution by bone marrow transplantation. RESULTS: Normal mice exhibited significant neutrophil infiltration into the esophagus as a result of acid-induced injury. The neutrophil accumulation was significantly diminished in mast cell-deficient mice. However, the neutrophil infiltration that resulted from acid-induced injury in mast cell-reconstituted Kit mice was similar to that seen in normal mice. CONCLUSIONS: Our findings provide direct evidence that mast cells participate in the recruitment of neutrophils during acid-induced esophageal injury in mice.

Original languageEnglish (US)
Pages (from-to)134-138
Number of pages5
JournalJournal of pediatric gastroenterology and nutrition
Volume46
Issue number2
DOIs
StatePublished - Feb 2008

Keywords

  • Acid reflux
  • Esophagitis
  • Inflammation
  • Mast cells

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Gastroenterology

Fingerprint Dive into the research topics of 'Direct evidence of mast cell participation in acute acid-induced esophageal inflammation in mice'. Together they form a unique fingerprint.

  • Cite this