title: Pulmonary periarterial inflammation in fatal asthma.
abstract: BACKGROUND
  To date, little information has been available about pulmonary artery pathology in asthma. The pulmonary artery supplies the distal parts of the lungs and likely represents a site of immunological reaction in allergic inflammation. The objective of this study was to describe the inflammatory cell phenotype of pulmonary artery adventitial inflammation in lung tissue from patients who died of asthma.
  
  
  METHODS
  We quantified the different inflammatory cell types in the periarterial region of small pulmonary arteries in lung tissue from 22 patients who died of asthma [fatal asthma (FA)] and 10 control subjects. Using immunohistochemistry and image analysis, we quantified the cell density for T lymphocytes (CD3, CD4, CD8), B lymphocytes (CD20), eosinophils, mast cells (chymase and tryptase), and neutrophils in the adventitial layer of pulmonary arteries with a diameter smaller than 500 microm.
  
  
  RESULTS
  Our data (median/interquartile range) demonstrated increased cell density of mast cells [FA=271.8 (148.7) cells/mm2; controls=177.0 (130.3) cells/mm2, P=0.026], eosinophils [FA=23.1 (58.6) cells/mm2; controls=0.0 (2.3) cells/mm2, P=0.012], and neutrophils [FA=50.4 (85.5) cells/mm2; controls=2.9 (30.5) cells/mm2, P=0.009] in the periarterial space in FA. No significant differences were found for B and T lymphocytes or CD4+ or CD8+ subsets. Chymase/tryptase positive (MCCT) mast cells predominated over tryptase (MCT) mast cells in the perivascular arterial space in both asthma patients and controls [MCCT/(MCCT+MCT)=0.91 (0-1) in FA and 0.75 (0-1) in controls, P=0.86].
  
  
  CONCLUSIONS
  Our results show that the adventitial layer of the pulmonary artery participates in the inflammatory process in FA, demonstrating increased infiltration of mast cells, eosinophils, and neutrophils, but not of T and B lymphocytes.
authors.affiliation: Department of Pathology, School of Medicine, São Paulo University, São Paulo, SP, Brazil.
authors.forename: C
authors.initials: C
authors.lastname: Shiang
authors.forename: T
authors.initials: T
authors.lastname: Mauad
authors.forename: A
authors.initials: A
authors.lastname: Senhorini
authors.forename: B B
authors.initials: BB
authors.lastname: de Araújo
authors.forename: D S
authors.initials: DS
authors.lastname: Ferreira
authors.forename: L F F
authors.initials: LF
authors.lastname: da Silva
authors.forename: M
authors.initials: M
authors.lastname: Dolhnikoff
authors.forename: M
authors.initials: M
authors.lastname: Tsokos
authors.forename: K F
authors.initials: KF
authors.lastname: Rabe
authors.forename: R
authors.initials: R
authors.lastname: Pabst
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000378:metabolism; D001167:Arteritis / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D001249:Asthma / Q000378:metabolism* / Q000401:mortality / Q000473:pathology; D002648:Child; D053818:Chymases / Q000378:metabolism; D005260:Female; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000401:mortality / Q000473:pathology; D007962:Leukocytes / Q000378:metabolism / Q000473:pathology; D008168:Lung / Q000098:blood supply / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008407:Mast Cells / Q000378:metabolism* / Q000473:pathology; D008875:Middle Aged; D011651:Pulmonary Artery / Q000378:metabolism* / Q000473:pathology; D012189:Retrospective Studies; D053802:Tryptases / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D053818:Chymases; D053802:Tryptases