Adhesion molecules and microvascular changes in the nonobese diabetic (NOD) mouse pancreas. An NO-inhibitor (L-Name) is unable to block adhesion inflammation-induced activation

Gianpaolo Papaccio, Michael V G Latronico, Francesco Aurelio Pisanti, Konrad Federlin, Thomas Linn

Research output: Contribution to journalArticle

Abstract

The aim of the present study was to investigate the immunoreactivity of pancreatic microvasculature with emphasis on the adhesion molecule expression in NOD mice at a very early stage and after the start of infiltration, before the onset of the diabetic disease. Immunoreactivity for Ia-b, BM8 (mouse macrophages) and inter-cellular-adhesion-molecule-1 (ICAM-1) molecules in untreated control mice and in animals treated using an inhibitor of nitric oxide (NO) formation (L-arginine analogue), as well as islet culture, nitrite assay and ultrastructural studies were performed. Results showed that Ia-b and ICAM-1 immunoreactivities on endothelia are a very early phenomenon and that pancreatic blood vessels and, in particular, some peri-islet venules, as well as several venules of the exocrine parenchyma, undergo significant morphological changes. Several endothelial cells of both peri-islet and extra-islet compartments, often showed Ia-b and ICAM-1 immunoreactivities, demonstrating that these cells are important for the adhesion processes taking place during early autoimmune inflammation. Inhibition of NO formation does not significantly affect ICAM-1 and Ia-b immunoreactivity both in vivo and in vitro, BM8 immunoreactive cells were considerably less in number although these were detected either around islets or along pancreatic septa, but rarely within the epithelial layer.

Original languageEnglish
Pages (from-to)65-77
Number of pages13
JournalAutoimmunity
Volume27
Issue number2
Publication statusPublished - 1998

Keywords

  • Adhesion molecules
  • Endothelium
  • NAME
  • NOD mice
  • Pancreatic islets

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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