Collagen and collagenase in occupational lung disease

Ronald Crystal, O. Kawanami, S. I. Rennard

Research output: Contribution to journalArticle

Abstract

It is apparent that the alveolar macrophage plays a central role in the pathogenesis of the fibrotic lung disorders associated with occupational exposures. While other effector cells contribute to the fibrotic process, it is the alveolar macrophage that, by virtue of its ability to expand the numbers of effector cells (i.e., neutrophils) and parenchymal cells (i.e., fibroblasts) within its local environment, can cause significant changes in the topologic organization of the alveolar structures. Through the process of neutrophil recruitment and activation, the macrophage effects major derangements to the alveolar connective tissue matrix. Furthermore, through its production of fibronectin and growth factor, the alveolar macrophage plays a central role in directing the reconstruction process by recruiting fibroblasts and expanding their numbers. In this context, fibrosis of the alveolar structures is similar to the process of scar formation following skin wounding. However, in the case of pulmonary fibrosis, the reconstruction process takes place within structures that have been so deranged by chronic inflammatory and immune processes that it is impossible to reestablish the architecture of the normal alveolar structures.

Original languageEnglish
Pages (from-to)85-94
Number of pages10
JournalJournal of UOEH
Volume4
Issue numberSuppl.
Publication statusPublished - 1 Jan 1982
Externally publishedYes

Fingerprint

Occupational Diseases
Alveolar Macrophages
Collagenases
Lung Diseases
Collagen
Fibroblasts
Neutrophil Activation
Neutrophil Infiltration
Pulmonary Fibrosis
Occupational Exposure
Fibronectins
Connective Tissue
Cicatrix
Neutrophils
Fibrosis
Cell Count
Macrophages
Lung
Skin
alveolar macrophage growth factor

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health

Cite this

Crystal, R., Kawanami, O., & Rennard, S. I. (1982). Collagen and collagenase in occupational lung disease. Journal of UOEH, 4(Suppl.), 85-94.

Collagen and collagenase in occupational lung disease. / Crystal, Ronald; Kawanami, O.; Rennard, S. I.

In: Journal of UOEH, Vol. 4, No. Suppl., 01.01.1982, p. 85-94.

Research output: Contribution to journalArticle

Crystal, R, Kawanami, O & Rennard, SI 1982, 'Collagen and collagenase in occupational lung disease', Journal of UOEH, vol. 4, no. Suppl., pp. 85-94.
Crystal R, Kawanami O, Rennard SI. Collagen and collagenase in occupational lung disease. Journal of UOEH. 1982 Jan 1;4(Suppl.):85-94.
Crystal, Ronald ; Kawanami, O. ; Rennard, S. I. / Collagen and collagenase in occupational lung disease. In: Journal of UOEH. 1982 ; Vol. 4, No. Suppl. pp. 85-94.
@article{ef8024e5b9fa45748f19d0f6d5b70857,
title = "Collagen and collagenase in occupational lung disease",
abstract = "It is apparent that the alveolar macrophage plays a central role in the pathogenesis of the fibrotic lung disorders associated with occupational exposures. While other effector cells contribute to the fibrotic process, it is the alveolar macrophage that, by virtue of its ability to expand the numbers of effector cells (i.e., neutrophils) and parenchymal cells (i.e., fibroblasts) within its local environment, can cause significant changes in the topologic organization of the alveolar structures. Through the process of neutrophil recruitment and activation, the macrophage effects major derangements to the alveolar connective tissue matrix. Furthermore, through its production of fibronectin and growth factor, the alveolar macrophage plays a central role in directing the reconstruction process by recruiting fibroblasts and expanding their numbers. In this context, fibrosis of the alveolar structures is similar to the process of scar formation following skin wounding. However, in the case of pulmonary fibrosis, the reconstruction process takes place within structures that have been so deranged by chronic inflammatory and immune processes that it is impossible to reestablish the architecture of the normal alveolar structures.",
author = "Ronald Crystal and O. Kawanami and Rennard, {S. I.}",
year = "1982",
month = "1",
day = "1",
language = "English",
volume = "4",
pages = "85--94",
journal = "Journal of UOEH",
issn = "0387-821X",
publisher = "University of Occupational and Environmental Health",
number = "Suppl.",

}

TY - JOUR

T1 - Collagen and collagenase in occupational lung disease

AU - Crystal, Ronald

AU - Kawanami, O.

AU - Rennard, S. I.

PY - 1982/1/1

Y1 - 1982/1/1

N2 - It is apparent that the alveolar macrophage plays a central role in the pathogenesis of the fibrotic lung disorders associated with occupational exposures. While other effector cells contribute to the fibrotic process, it is the alveolar macrophage that, by virtue of its ability to expand the numbers of effector cells (i.e., neutrophils) and parenchymal cells (i.e., fibroblasts) within its local environment, can cause significant changes in the topologic organization of the alveolar structures. Through the process of neutrophil recruitment and activation, the macrophage effects major derangements to the alveolar connective tissue matrix. Furthermore, through its production of fibronectin and growth factor, the alveolar macrophage plays a central role in directing the reconstruction process by recruiting fibroblasts and expanding their numbers. In this context, fibrosis of the alveolar structures is similar to the process of scar formation following skin wounding. However, in the case of pulmonary fibrosis, the reconstruction process takes place within structures that have been so deranged by chronic inflammatory and immune processes that it is impossible to reestablish the architecture of the normal alveolar structures.

AB - It is apparent that the alveolar macrophage plays a central role in the pathogenesis of the fibrotic lung disorders associated with occupational exposures. While other effector cells contribute to the fibrotic process, it is the alveolar macrophage that, by virtue of its ability to expand the numbers of effector cells (i.e., neutrophils) and parenchymal cells (i.e., fibroblasts) within its local environment, can cause significant changes in the topologic organization of the alveolar structures. Through the process of neutrophil recruitment and activation, the macrophage effects major derangements to the alveolar connective tissue matrix. Furthermore, through its production of fibronectin and growth factor, the alveolar macrophage plays a central role in directing the reconstruction process by recruiting fibroblasts and expanding their numbers. In this context, fibrosis of the alveolar structures is similar to the process of scar formation following skin wounding. However, in the case of pulmonary fibrosis, the reconstruction process takes place within structures that have been so deranged by chronic inflammatory and immune processes that it is impossible to reestablish the architecture of the normal alveolar structures.

UR - http://www.scopus.com/inward/record.url?scp=0020318556&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020318556&partnerID=8YFLogxK

M3 - Article

VL - 4

SP - 85

EP - 94

JO - Journal of UOEH

JF - Journal of UOEH

SN - 0387-821X

IS - Suppl.

ER -