The contribution of type II pneumocytes and alveolar macrophages to fibroplasia processes in the course of enzymatic lung injury

被引:0
作者
Sulkowska, M
Sulkowski, S
机构
关键词
emphysema; fibrosis; type II pneumocyte;
D O I
暂无
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The aim of the paper was to evaluate mutual relations in the system of alveolar macrophage (AM) type II 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 focal 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 H-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 H-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.
引用
收藏
页码:111 / 122
页数:12
相关论文
共 33 条
  • [1] ADAMSON IYR, 1988, AM J PATHOL, V130, P377
  • [2] BECKSTEAD JH, 1981, BLOOD, V57, P1088
  • [3] COLLAGEN AND ELASTIN IN HUMAN PULMONARY-EMPHYSEMA
    CARDOSO, WV
    SEKHON, HS
    HYDE, DM
    THURLBECK, WM
    [J]. AMERICAN REVIEW OF RESPIRATORY DISEASE, 1993, 147 (04): : 975 - 981
  • [4] ENDOTOXIN-INDUCED SERUM FACTOR THAT CAUSES NECROSIS OF TUMORS
    CARSWELL, EA
    OLD, LJ
    KASSEL, RL
    GREEN, S
    FIORE, N
    WILLIAMSON, B
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1975, 72 (09) : 3666 - 3670
  • [5] CHYCZEWSKA E, 1993, FOLIA HISTOCHEM CYTO, V31, P113
  • [6] CLARK JG, 1987, AM REV RESPIR DIS, V135, P52
  • [7] CROUCH EC, 1987, AM REV RESPIR DIS, V135, P1118
  • [8] TURNOVER OF EXTRACELLULAR-MATRIX BY TYPE-II PULMONARY EPITHELIAL-CELLS
    DUNSMORE, SE
    RANNELS, DE
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1995, 268 (02) : L336 - L346
  • [9] ALKALINE-PHOSPHATASE - A MARKER OF ALVEOLAR TYPE-II CELL-DIFFERENTIATION
    EDELSON, JD
    SHANNON, JM
    MASON, RJ
    [J]. AMERICAN REVIEW OF RESPIRATORY DISEASE, 1988, 138 (05): : 1268 - 1275
  • [10] ESCOLAR JD, 1995, HISTOL HISTOPATHOL, V10, P875