Changes in the ultrastructure of feline pulmonary arteries following infection with the lungworm Aelurostrongylus abstrusus |
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| Affiliation: | 1. Hôpital Universitaire de Bicêtre, Université Paris Sud, Le Kremlin-Bicêtre, France;2. UT Southwestern Medical Center, Dallas, Texas;3. University of California, Los Angeles, Los Angeles, California;4. Allegheny General Hospital, Pittsburgh, Pennsylvania;5. Actelion Pharmaceuticals Ltd, Allschwil, Switzerland;6. National Pulmonary Hypertension Unit, Mater Misericordiae University Hospital, Dublin, Ireland;7. University of Giessen and Marburg Lung Center, member of the German Center of Lung Research, Giessen, Germany;8. Department of Medicine, Imperial College London, London, United Kingdom;9. Department of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Allgemeines Krankenhaus, Vienna, Austria;10. Department of Internal Medicine, Division of Cardiovascular Medicine, University of Michigan, Ann Arbor, Michigan;11. Division of Pulmonary and Critical Care Medicine, University of California, San Diego, California;12. Cedars-Sinai Medical Center, Los Angeles, California;13. Department of Experimental, Diagnostic and Specialty Medicine – DIMES, University of Bologna, Bologna, Italy;14. Department of Respiratory Medicine and German Center of Lung Research, Hannover Medical School, Hannover, Germany;1. Laboratorio di Parassitologia, Ospedale Didattico Veterinario, Dipartimento di Medicina Veterinaria, Università degli Studi di Sassari, Italy;2. Dipartimento di Scienze Veterinarie, Università degli Studi di Messina, Messina, Italy |
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| Abstract: | A study was made of the ultrastructural changes which occur in feline pulmonary arteries as a consequence of experimental infection with the lungworm Aelurostrongylus abstrusus.Pulmonary tissue was studied at intervals from 10 days to 24 weeks post infection. There was progressive disruption of the vascular endothelium resulting in vacuolation and later proliferation of the endothelial cells. Eosinophils were observed migrating through the artery walls as early as 10 days post infection, resulting in disruption of the internal elastic laminae and contributing to the disruption of the endothelium. Hypertrophy and hyperplasia of the smooth muscle cells of the media were evident and this, together with intimai proliferation, resulted in complete occlusion of the lumen of many of the vessels by 24 weeks post infection. Immunofluorescence failed to reveal any evidence of immune complex deposition in pulmonary vasculature or parenchyma at any stage of the infestation. The possible role of endogenous vasoactive compounds in the genesis of the lesion is discussed. |
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