title: PTX3 expression in the heart tissues of patients with myocardial infarction and infectious myocarditis.
abstract: BACKGROUND
  The long pentraxin 3 is involved in innate resistance to pathogens, controlling inflammation and extracellular matrix remodeling. Moreover, pentraxin 3 plays a nonredundant role in the regulation of cardiac tissue damage in mice and, recently, it has been proposed as a new candidate marker for acute and chronic heart diseases. However, the actual localization and cellular sources of pentraxin 3 in ischemic and infectious cardiac pathology have not been carefully defined.
  
  
  METHODS
  In this study, using immunohistochemistry, we analyzed pentraxin 3 expression in the heart tissues of patients with acute myocardial infarction at different time points after the ischemic event. In addition, we studied the heart tissues of patients with infectious myocarditis (fungi, bacteria, and protozoa) and patients who died of noncardiac events with normal heart histology.
  
  
  RESULTS
  In acute myocardial infarction cases, we observed pentraxin 3 localized within and around ischemic lesions. On the contrary, no pentraxin 3 was observed in normal heart areas. In early ischemic lesions, pentraxin 3 was localized primarily in granulocytes; in more advanced acute myocardial infarction, pentraxin 3 positivity was found in the interstitium and in the cytoplasm of macrophages and the endothelium, whereas most granulocytes did not express pentraxin 3, presumably as a consequence of degranulation. In infectious myocarditis, pentraxin 3 was present and localized within and around histological lesions, associated with macrophage, endothelial cell, and, more rarely, myocardiocyte and granulocyte positivities. As observed in acute myocardial infarction patients, no pentraxin 3 staining was found in normal heart areas.
  
  
  CONCLUSIONS
  Thus, neutrophils are an early source of pentraxin 3 in acute myocardial infarction and presumably other inflammatory heart disorders. Subsequently, in acute myocardial infarction and infectious myocarditis, pentraxin 3 is produced by macrophages, the endothelium, and, to a lesser extent, myocardiocytes, and localized in the interstitium.
authors.affiliation: Pathology Unit, L. Sacco Department of Clinical Sciences, L. Sacco Hospital, Università degli Studi di Milano, Milan, Italy.
authors.forename: Manuela
authors.initials: M
authors.lastname: Nebuloni
authors.forename: Fabio
authors.initials: F
authors.lastname: Pasqualini
authors.forename: Pietro
authors.initials: P
authors.lastname: Zerbi
authors.forename: Eleonora
authors.initials: E
authors.lastname: Lauri
authors.forename: Alberto
authors.initials: A
authors.lastname: Mantovani
authors.forename: Luca
authors.initials: L
authors.lastname: Vago
authors.forename: Cecilia
authors.initials: C
authors.lastname: Garlanda
mesh_terms: D001424:Bacterial Infections / Q000378:metabolism / Q000473:pathology; D015415:Biomarkers / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism*; D016022:Case-Control Studies; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology; D005260:Female; D006098:Granulocytes / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D008264:Macrophages / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009181:Mycoses / Q000378:metabolism / Q000473:pathology; D009203:Myocardial Infarction / Q000378:metabolism* / Q000473:pathology; D009205:Myocarditis / Q000378:metabolism* / Q000473:pathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D000683:Serum Amyloid P-Component / Q000378:metabolism*; D013997:Time Factors; D014123:Toxoplasmosis / Q000378:metabolism / Q000473:pathology; D014381:Tuberculosis, Cardiovascular / Q000378:metabolism / Q000473:pathology; D000099153:Pentraxins
chemical_list: D015415:Biomarkers; D002097:C-Reactive Protein; D000683:Serum Amyloid P-Component; D000099153:Pentraxins