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Departments of Medicine,
Cell Biology and Anatomy, Pediatrics and Ophthalmology, Oregon Health
Sciences University, Portland, Oregon 97201-3098, USA
Correspondence to: Dr J M Liebler, Pulmonary and Critical Care Medicine Division, Oregon Health Sciences University UHN-67, 3181 S W Sam Jackson Park Road, Portland, Oregon 97201-3098, USA.
Received 24 September 1997; Returned to authors 11 December 1997; Revised version received 25 March 1998; Accepted for publication 26 May 1998
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.
METHODSLung 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), 
-smooth muscle
actin (identifies myofibroblasts), and procollagen type I was performed.
RESULTSNormal 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 
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.
CONCLUSIONSIncreased 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.
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