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Macrophage Phenotype Is Associated With the Regenerative Response in Experimental Replacement of the Porcine Esophagus.

Journal article
Authors Linus Jönsson
Michaela Dellenmark-Blom
Lars-Göran Friberg
Vladimir Gatzinsky
Olof Holmquist
Eva Jennische
Anders Sandin
Kate Abrahamsson
Published in Artificial organs
Volume 40
Issue 10
Pages 950-958
ISSN 1525-1594
Publication year 2016
Published at Institute of Clinical Sciences, Department of Pediatrics
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages 950-958
Language en
Links dx.doi.org/10.1111/aor.12652
Subject categories Pediatrics

Abstract

A porcine model for bridging circumferential defects in the intrathoracic esophagus has been developed in order to improve the treatment of children born with long-gap esophageal atresia. The aim of this study was to identify factors beneficial for tissue regeneration in the bridging area in this model and to describe the histological progression 20 days after replacement with a silicone-stented Biodesign mesh. Resection of 3 cm of intrathoracic esophagus and replacement with a bridging graft was performed in six newly weaned piglets. They were fed through a gastrostomy for 10 days, and then had probe formula orally for another 10 days prior to sacrifice. Two out of six piglets had stent loss prior to sacrifice. In the four piglets with the stent in place, a tissue tube, with visible muscle in the wall, was seen at sacrifice. Histology showed that the wall of the healing area was well organized with layers of inflammatory cells, in-growing vessels, and smooth muscle cells. CD163+ macrophages was seen toward the esophageal lumen. In the animals where the stent was lost, the bridging area was narrow, and histology showed a less organized structure in the bridging area without the presence of CD163+ macrophages. This study indicates that regenerative healing was seen in the porcine esophagus 20 days after replacement of a part of the intrathoracic esophagus with a silicone-stented Biodesign mesh, if the bridging graft is retained. If the graft is lost, the inflammatory pattern changes with invasion of proinflammatory, M1 macrophages in the entire wall, which seems to redirect the healing process toward scar formation.

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