Expression of Adhesion Molecules in a Gastroduodenal Reflux Murine Model.

BACKGROUND: Various adhesion molecules, including intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), have been shown to play a role in inflammation as well as contribute to tumor progression and prognosis. We hypothesized that gastroduodenal reflux upregulates ICAM-1 and VCAM-1 expression in the distal esophagus, serving as possible early markers of pathologic esophageal disease. METHODS: Normal human esophageal epithelial cells (HET1A), Barrett cells (CPB), and esophageal adenocarcinoma cells (FLO1 and OE33) were treated with deoxycholic acid at increasing concentrations for 24 hours. Adhesion molecule expression was assessed using immunoblotting. A surgical mouse reflux model was generated by performing a side-to-side anastomosis between the gastroesophageal junction and the first portion of the duodenum (duodenum-gastroesophageal anastomosis). Esophageal sections were evaluated using hematoxylin and eosin staining, immunohistochemistry, and immunofluorescence. RESULTS: Deoxycholic acid induced a significant increase in ICAM-1 and VCAM-1 expression in HET1A, CPB, FLO1, and OE33 cells. Animals undergoing duodenum-gastroesophageal anastomosis demonstrated a significant increase in mucosal hyperplasia (P < .0001) and cellular proliferation (P < .0001) compared with control animals. Immunofluorescence and Western blot analysis of the lower esophagus demonstrated significant upregulation of ICAM-1 (P = .005), with no change in VCAM-1 expression (P = .82). CONCLUSIONS: Our results reveal that ICAM-1 and VCAM-1 are upregulated in response to in vitro reflux treatment of normal esophageal epithelial cells. However, our investigation using a mouse reflux model found ICAM-1 is noticeably upregulated without a concomitant increase in VCAM-1. These findings identify ICAM-1, but not VCAM-1, as a potential player in early esophageal disease developing from chronic reflux exposure.

Coronavirus Disease 2019 in Lung Transplant Recipients.

We report risk factors, clinical manifestations, and treatment course of 2 lung transplant recipients diagnosed with coronavirus disease 2019 (COVID-19) pneumonia. Both patients underwent an initial hospitalization and discharged home, followed by readmission several days later with significant worsening of respiratory status and infectious symptoms. The first patient underwent prolonged hospitalization requiring tracheostomy and feeding tube placement. The second patient declined intubation and expired. The early documented experiences of COVID-19 pneumonia in lung transplant recipients suggest that although recovery is achievable, the high rate of comorbid conditions and immunocompromised state may place these patients at higher risk for poor outcomes.