title: Decreased numbers of T-lymphocytes and predominance of recently recruited macrophages in the walls of peripheral pulmonary arteries from 26 patients with pulmonary hypertension secondary to congenital cardiac shunts.
abstract: BACKGROUND
  In the primary form of pulmonary hypertension (PH), the involvement of inflammation in the physiopathology of the vascular lesions is well established. Its role in secondary PH is yet to be investigated. We quantified the inflammatory cells on the walls of peripheral pulmonary arteries from patients with congenital heart shunts.
  
  
  METHODS
  Twenty-six lung biopsies from patients with increased pulmonary flow and 10 lung fragments from control participants were examined. B-lymphocytes (CD20), T-lymphocytes (CD3), recently recruited macrophages (MAC387) and granulocytes (CD15) were quantified by area of the adventitia in arteries >50 microm. An index of inflammatory cells infiltrating the medial and intimal layers was also determined.
  
  
  RESULTS
  There was no difference in the sum of densities of adventitial inflammatory cells between the groups. A prevalence of MAC387-labeled cells was detected in the PH group and of CD3-labeled cells in the controls. There was a lower density of T-lymphocytes in the PH group (P<.004). Patients with intimal proliferative lesions showed prevalence of MAC387-labeled cells (P=.004). PH participants showed a higher index of MAC387-labeled cells infiltrating the arterial medial and intimal layers (P<.001).
  
  
  CONCLUSIONS
  The predominance of recently recruited macrophages in the PH group is compatible with ongoing inflammatory reaction in the arterial walls. This could be related to the pathogenesis of the vascular lesions, as a consequence of cytokines produced by the inflammatory cells. The smaller number of adventitial T-lymphocytes in patients with congenital shunts can reflect an impairment of their immune response.
authors.affiliation: Laboratory of Pathology, Heart Institute (InCor), São Paulo University Medical School, Av. Dr. Enéas C. Aguiar 44, São Paulo-SP 05403-000, Brazil.
authors.forename: Rubens Fraga Alves
authors.initials: RF
authors.lastname: Pinto
authors.forename: Maria de Lourdes
authors.initials: Mde L
authors.lastname: Higuchi
authors.forename: Vera Demarchi
authors.initials: VD
authors.lastname: Aiello
mesh_terms: D018951:Antigens, CD20 / Q000276:immunology; D015415:Biomarkers / Q000032:analysis; D017252:CD3 Complex / Q000276:immunology; D002423:Cause of Death; D002648:Child; D002675:Child, Preschool; D005260:Female; D006330:Heart Defects, Congenital / Q000150:complications / Q000276:immunology / Q000473:pathology*; D006801:Humans; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000276:immunology / Q000473:pathology*; D007223:Infant; D008264:Macrophages / Q000276:immunology / Q000473:pathology*; D008297:Male; D011651:Pulmonary Artery / Q000276:immunology / Q000473:pathology*; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology*
chemical_list: D018951:Antigens, CD20; D015415:Biomarkers; D017252:CD3 Complex