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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2 Pt 1
|
| pubmed:dateCreated |
1989-9-15
|
| pubmed:abstractText |
In the last 10 years there has been an increased appreciation of the changes in lung cell populations that occur in association with the acute respiratory failure often induced by traumatic injury. Early events result in an accumulation in the lung of platelets, neutrophils, monocytes, and macrophages, a release of substances having potent cardiopulmonary and metabolic effects, and an ensuing edema and transudation of materials from the interstitium and capillaries into the alveoli. Further progression of the injury results in significant decreases in the number of endothelial and type I epithelial cells and a subsequent hyperplasia of fibroblasts and type II-like epithelial cells. Major sequelae of the latter stage of the disease are interstitial and interalveolar fibrosis, probably resulting from the increased number of fibroblasts present. The activity and composition of pulmonary surfactant are often perturbed. This review will discuss mechanisms that may be involved in these processes, with major emphasis on cell-cell interactions mediated through polypeptide growth factors. We describe the properties of certain growth factors commonly associated with inflammatory and wound healing reactions, discuss their cellular origins, and speculate on their possible roles in mediating the structural and physiological responses seen in the lung during acute respiratory failure. The majority of work done with lung cells has concentrated on interactions between macrophages and fibroblasts, and it is evident that macrophages are capable of producing mitogens affecting the proliferation of fibroblasts. However, from the results of studies that are less developed, it is possible that epithelial cells and immunologically stimulated cells could also be involved in these actions. We conclude that the homeostasis of lung cell populations may be influenced by both growth-stimulating and growth-inhibiting substances and potentially could involve interactions through growth factors of fibroblasts, macrophages, lymphocytes, alveolar epithelial cells, endothelial cells, and platelets. At this time the information on these purported interactions is quite limited and there are far more questions than answers.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Aug
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| pubmed:issn |
0002-9513
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
257
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
L23-38
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| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading | |
| pubmed:year |
1989
|
| pubmed:articleTitle |
Regulation of lung cell proliferation by polypeptide growth factors.
|
| pubmed:affiliation |
Department of Physiology, University of Texas Health Science Center, San Antonio 78284.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Review
|