title: Inflammatory cell phenotyping of the pulmonary interstitium in idiopathic interstitial pneumonia.
abstract: BACKGROUND
  Several studies have implicated the role of inflammation in the pathogenesis of lung damage in idiopathic interstitial pneumonias (IIPs). Investigations of inflammatory cells in IIP have show that eosinophils, neutrophils and T cells may be associated with a poorer prognosis.
  
  
  OBJECTIVE
  The aim of our study was to map, by quantitative analysis, the number of inflammatory cells in the lung tissue of patients with non-specific interstitial pneumonia/non-specific interstitial pneumonia (NSIP/NSIP), acute interstitial pneumonia/diffuse alveolar damage (AIP/DAD) and idiopathic pulmonary fibrosis/usual interstitial pneumonia (IPF/UIP) and to correlate them with lung function tests and survival.
  
  
  METHODS
  After immunohistochemical staining, we quantified the content of inflammatory cells [macrophages, neutrophils (elastase+), plasma cells, and CD3, CD4 and CD8 T lymphocytes (TLs)] in 20 NSIP, 20 DAD and 20 UIP surgical lung biopsies.
  
  
  RESULTS
  The total density of inflammatory cells was significantly increased in DAD and NSIP when compared to UIP (p = 0.04). TLs were increased in DAD and NSIP when compared to UlP lungs (p < 0.05). The density of inflammatory cells in UIP showed significant differences in normal, intervening and dense fibrosis areas (p < 0.05). The most numerous cells infiltrating the mural fibrosis and honeycombing areas were plasma cells, neutrophils (elastase+), CD20+, CD3+, CD4+ and CD8+ (p < 0.05). In UIP, CD3+ TLs were directly correlated with forced expiratory volume in 1 s/forced vital capacity ratio x 100 (p = 0.05). CD68+ cells presented a significant positive correlation with the forced expiratory volume in 1 s (p = 0.04); neutrophil (elastase+) cells significantly correlated with residual volume (p = 0.02), residual volume/total lung capacity (p = 0.04) and carbon monoxide transfer factor (p = 0.03). The most important predictor of survival in UIP was CD3+ TLs (p = 0.05).
  
  
  CONCLUSIONS
  The total density of inflammatory cells and lymphocytes presents a different distribution within the pulmonary parenchyma in AIP/DAD, NSIP/NSIP and IPF/UIP evolutionary adapted responses to injury. There is a localized distribution of inflammation in the normal, intervening and dense fibrosis areas of UIP for CD3+, associated with a lethal deterioration of the pulmonary function and poor survival. Our findings provide further evidence of the importance of inflammation in the pathophysiology of IIPs.
authors.affiliation: Department of Pathology, School of Medicine, University of São Paulo, São Paulo, Brazil.
authors.forename: Edwin Roger
authors.initials: ER
authors.lastname: Parra
authors.forename: Ronaldo Adib
authors.initials: RA
authors.lastname: Kairalla
authors.forename: Carlos Roberto
authors.initials: CR
authors.lastname: Ribeiro de Carvalho
authors.forename: Esmeralda
authors.initials: E
authors.lastname: Eher
authors.forename: Vera Luiza
authors.initials: VL
authors.lastname: Capelozzi
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001706:Biopsy; D002452:Cell Count; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000473:pathology*; D007963:Leukocytes, Mononuclear / Q000473:pathology*; D017563:Lung Diseases, Interstitial / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D011379:Prognosis; D020545:Respiratory Mucosa / Q000473:pathology*; D012720:Severity of Illness Index; D014057:Tomography, X-Ray Computed