title: Emergence of inflammatory alveolar macrophages during rejection or infection after lung transplantation.
abstract: Local activation of macrophages may play an important role in immune complications following lung transplantation. To document such a phenomenon, we have investigated the possible changes of alveolar macrophage surface antigen expression after lung transplantation. Using immunocytofluorometry, we have analyzed the phenotype of alveolar macrophages from 41 bronchoalveolar lavage fluids obtained from 19 lung transplant recipients displaying various complications. The strong expression of HLA-DR observed on almost all alveolar macrophages was similar among groups I (no complication), II (minimal acute rejection), and III (mild to severe acute rejection), but was enhanced in group IV (bronchial infection) (P < 0.03). We observed no significant variation in the monocyte lineage CD14 antigen expression among the 4 groups, and about 83% of alveolar macrophages expressed this marker strongly. Membrane expression of the 27E10 antigen that characterizes infiltrating macrophages in acute inflammatory lesions was significantly higher during mild to severe rejection episodes than in controls (P < 0.02) and during bronchial infections (P < 0.05) but not during minimal rejection. Double staining experiments confirmed that 27E10-positive cells in groups III and IV belonged to the macrophage lineage. In addition, the expression of the 27E10 antigen on cultured alveolar macrophages was found to be increased after stimulation by bacterial lipopolysaccharide or IFN-gamma. These results indicate that a particular alveolar macrophage subpopulation is activated during immune events after lung transplantation. This population, recognized by the 27E10 mAb, might be involved in cytokine production during severe acute rejection and infection episodes.
authors.affiliation: Laboratory of Immunology, CNRS URA-1159, Hôpital Marie-Lannelongue, Le Plessis-Robinson, France.
authors.forename: I
authors.initials: I
authors.lastname: Frachon
authors.forename: M
authors.initials: M
authors.lastname: Fattal-German
authors.forename: A
authors.initials: A
authors.lastname: Magnan
authors.forename: J
authors.initials: J
authors.lastname: Cerrina
authors.forename: F
authors.initials: F
authors.lastname: Le Roy Ladurie
authors.forename: F
authors.initials: F
authors.lastname: Parquin
authors.forename: B
authors.initials: B
authors.lastname: Rain
authors.forename: F
authors.initials: F
authors.lastname: Lecerf
authors.forename: P
authors.initials: P
authors.lastname: Dartevelle
authors.forename: D
authors.initials: D
authors.lastname: Emilie
mesh_terms: D000293:Adolescent; D000328:Adult; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D005260:Female; D006084:Graft Rejection; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D007239:Infections / Q000276:immunology; D018950:Lipopolysaccharide Receptors; D016040:Lung Transplantation / Q000009:adverse effects* / Q000276:immunology; D016676:Macrophages, Alveolar / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D010641:Phenotype
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D006684:HLA-DR Antigens; D018950:Lipopolysaccharide Receptors