Cargando…

Control of cellular influx in lung and its role in pulmonary toxicology.

The pulmonary influx of cytotoxic inflammatory cells, normally, in response to external toxins, is now thought to be etiologic in many of the disease syndromes of man, such as bronchitis and emphysema. Many types of effector inflammatory cells are involved, e.g., eosinophils, neutrophils, T-lymphocy...

Descripción completa

Detalles Bibliográficos
Autor principal: Lynn, W S
Formato: Texto
Lenguaje:English
Publicado: 1984
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1568375/
https://www.ncbi.nlm.nih.gov/pubmed/6376103
_version_ 1782130000302964736
author Lynn, W S
author_facet Lynn, W S
author_sort Lynn, W S
collection PubMed
description The pulmonary influx of cytotoxic inflammatory cells, normally, in response to external toxins, is now thought to be etiologic in many of the disease syndromes of man, such as bronchitis and emphysema. Many types of effector inflammatory cells are involved, e.g., eosinophils, neutrophils, T-lymphocytes, monocytes. The diseases are characterized either by tissue destruction or by tissue hyperplasia. Agents which initiate the influx and cytotoxic secretions by these cells are legion and in general are not cell-specific. They include agents, such as phorbol esters, formyl peptides-complement fragments, elastin fragments, fatty acids (leukotrienes) as well as many uncharacterized excretions of inflammatory cells themselves, which react with specific receptors on the inflammatory cells, and secreted proteins such as fibronectin. Other agents, such as linoleic acid, digitonin and hydroxy fatty acids which are not bound by specific receptors also activate motility of inflammatory cells. The precise role of the above multiple cytotoxins in specific cellular fluxes in most pulmonary disease remains undefined. Similarly, the mechanism of cytotoxicity used by specific invading cells in specific pulmonary syndromes remains unclear. In general, macrophages are thought to destroy using specific proteases, neutrophils use oxidant radicals and proteases and eosinophils use basic surface active peptides. T-cells kill by unknown mechanisms. However, in specific clinical syndromes, it is usually not clear which cell is the cytotoxic culprit, nor is the mechanism of destruction usually known.
format Text
id pubmed-1568375
institution National Center for Biotechnology Information
language English
publishDate 1984
record_format MEDLINE/PubMed
spelling pubmed-15683752006-09-18 Control of cellular influx in lung and its role in pulmonary toxicology. Lynn, W S Environ Health Perspect Research Article The pulmonary influx of cytotoxic inflammatory cells, normally, in response to external toxins, is now thought to be etiologic in many of the disease syndromes of man, such as bronchitis and emphysema. Many types of effector inflammatory cells are involved, e.g., eosinophils, neutrophils, T-lymphocytes, monocytes. The diseases are characterized either by tissue destruction or by tissue hyperplasia. Agents which initiate the influx and cytotoxic secretions by these cells are legion and in general are not cell-specific. They include agents, such as phorbol esters, formyl peptides-complement fragments, elastin fragments, fatty acids (leukotrienes) as well as many uncharacterized excretions of inflammatory cells themselves, which react with specific receptors on the inflammatory cells, and secreted proteins such as fibronectin. Other agents, such as linoleic acid, digitonin and hydroxy fatty acids which are not bound by specific receptors also activate motility of inflammatory cells. The precise role of the above multiple cytotoxins in specific cellular fluxes in most pulmonary disease remains undefined. Similarly, the mechanism of cytotoxicity used by specific invading cells in specific pulmonary syndromes remains unclear. In general, macrophages are thought to destroy using specific proteases, neutrophils use oxidant radicals and proteases and eosinophils use basic surface active peptides. T-cells kill by unknown mechanisms. However, in specific clinical syndromes, it is usually not clear which cell is the cytotoxic culprit, nor is the mechanism of destruction usually known. 1984-04 /pmc/articles/PMC1568375/ /pubmed/6376103 Text en
spellingShingle Research Article
Lynn, W S
Control of cellular influx in lung and its role in pulmonary toxicology.
title Control of cellular influx in lung and its role in pulmonary toxicology.
title_full Control of cellular influx in lung and its role in pulmonary toxicology.
title_fullStr Control of cellular influx in lung and its role in pulmonary toxicology.
title_full_unstemmed Control of cellular influx in lung and its role in pulmonary toxicology.
title_short Control of cellular influx in lung and its role in pulmonary toxicology.
title_sort control of cellular influx in lung and its role in pulmonary toxicology.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1568375/
https://www.ncbi.nlm.nih.gov/pubmed/6376103
work_keys_str_mv AT lynnws controlofcellularinfluxinlunganditsroleinpulmonarytoxicology