Fibroproliferation and mast cells in the acute respiratory distress syndrome.
BACKGROUND
Mast cells (MCs), which are a major source of cytokines and growth factors, have been implicated in various fibrotic disorders. To clarify the contribution of MCs to fibrogenesis, lung tissue from patients with the acute respiratory distress syndrome (ARDS) was examined during exudative through to fibroproliferative stages.


METHODS
Lung tissue was obtained from 17 patients with ARDS who had pathological features of the early exudative stage (n = 6) or the later reparative stages (n = 11), from four patients with idiopathic pulmonary fibrosis, and from three patients with normal lung tissue. Immunohistochemical localisation of tryptase (found in all human MCs), chymase (found in a subset of human MCs), alpha-smooth muscle actin (identifies myofibroblasts), and procollagen type I was performed.


RESULTS
Normal lung tissue exhibited myofibroblast and procollagen type I immunolocalisation scores each of < 5 and MC scores of 1. Increased scores were defined as myofibroblast and procollagen type I scores of > 10 and MC scores of > or = 2. Eighty percent of lung tissue samples from the early exudative stage of ARDS exhibited increased numbers of myofibroblasts, 50% had increased numbers of procollagen type I producing cells, while only 17% had increased numbers of MCs compared with control samples. All samples from the later reparative stages of ARDS had increased numbers of myofibroblasts and procollagen type I producing cells. Increased numbers of MCs were seen in 55% of samples from the reparative stages. There was no significant shift in MC phenotype in the ARDS samples.


CONCLUSIONS
Increased numbers of myofibroblasts and procollagen type I producing cells were frequently found early in the course of ARDS. MC hyperplasia was unusual during this stage, but was often a feature of the later reparative stages. MCs do not appear to initiate fibroproliferation in ARDS.
Liebler
J M
JM
Department of Medicine, Oregon Health Sciences University, Portland 97201-3098, USA.
Qu
Z
Z
Buckner
B
B
Powers
M R
MR
Rosenbaum
J T
JT
D000199:Actins / Q000032:analysis; D002452:Cell Count; D053818:Chymases; D005347:Fibroblasts / Q000473:pathology; D005355:Fibrosis; D006801:Humans; D007150:Immunohistochemistry; D018836:Inflammation Mediators / Q000032:analysis; D008168:Lung / Q000276:immunology / Q000473:pathology*; D008407:Mast Cells / Q000473:pathology*; D011347:Procollagen / Q000032:analysis; D011658:Pulmonary Fibrosis / Q000276:immunology / Q000473:pathology; D012128:Respiratory Distress Syndrome / Q000276:immunology / Q000473:pathology*; D012697:Serine Endopeptidases / Q000032:analysis; D018709:Statistics, Nonparametric; D053802:Tryptases
D000199:Actins; D018836:Inflammation Mediators; D011347:Procollagen; D012697:Serine Endopeptidases; C083294:chymase 2; D053818:Chymases; D053802:Tryptases