Publication: The contribution of type II pneumocytes and alveolar macrophages to fibroplasia processes in the course of enzymatic lung injury
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Date
1997
Authors
Sulkowska, M. ; Sulkowski, S.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The aim of the paper was to evaluate mutual
relations in the system of alveolar macrophage (AM) -
type 11 pneumocyte (PII) - interstitium of alveolar septa,
in the course of experimental lung emphysema in rats
subjected to BCG vaccine effect.
Administration of BCG vaccine resulted in the
cumulation of AM within pulmonary alveoli. These cells
exhibited morphological features of increased activity.
Intratracheal papain injection induced intralobular
emphysema changes, partly generalized, in the animal
lungs. The emphysematous changes, with domination of
interalveolar septum atrophy, were accompanied by
foca1 accumulation of collagen and elastin. Fibroplasia
processes were strongly pronounced in BCG- and
papain-treated animals. The areas of connective tissue
fibres cumulation revealed indistinctness of the
boundary line between PII and the interstitium in some
places. Anchorage of collagen fibres and microfibrillary
structures were observed in the cytoplasm of PII.
The morphological examinations of AM - fibroblasts
co-cultures as well as the evaluation of the uptake of 3 ~ -
thymidine did not show any significant differences
between respective co-cultures of fibroblasts and AM
isolated both from the lungs of control and experimental
animals (treated with BCG or papain, and BCG+papain).
However, a significant growth was noted in 3 ~ -
thymidine uptake between fibroblast cultures realized
with or without cells isolated from the lungs.
The results obtained suggest the possibility of active participation of PII and AM in fibroplasia processes in
the course of lung rebuilding after papain administration
and in pathological states of the pulmonary tissue,
particularly when they are accompanied by increased
activity of alveolar macrophages. They also support the
inflammatory-repair hypothesis in the development of
emphysematous changes.
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