The Sources of Inflammatory Mediators in the Lung after Silica Exposure

By Porter, Dale W.

Book Id: WPLBN0000187255
Format Type: PDF eBook:
File Size: 0.2 MB
Reproduction Date: 2005

Title:	The Sources of Inflammatory Mediators in the Lung after Silica Exposure
Author:	Porter, Dale W.
Volume:
Language:	English
Subject:	Government publications, United Nations., United Nations. Office for Disarmament Affairs
Collections:	Government Library Collection, Disarmament Documents
Historic Publication Date:
Publisher:	United Nations- Office for Disarmament Affairs (Unoda)


Citation APA MLA Chicago W. Porte, B. D. (n.d.). The Sources of Inflammatory Mediators in the Lung after Silica Exposure. Retrieved from https://www.gutenberg.us/

Description
Government Reference Publication

Excerpt
Excerpt: The expression of 10 genes implicated in regulation of the inflammatory processes in the lung was studied after exposure of alveolar macrophages (AMs) to silica in vitro or in vivo. Exposure of AMs to silica in vitro up-regulated the messenger RNA (mRNA) levels of three genes [interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and macrophage inflammatory protein-2 (MIP-2)] without a concomitant increase in the protein levels. AMs isolated after intratracheal instillation of silica up-regulated mRNA levels of four additional genes [granulocyte/macrophagecolony stimulating factor (GM-CSF), IL-1(Beta), IL-10, and inducible nitric oxide synthase]. IL-6, MCP-1, and MIP-2 protein levels were elevated in bronchoalveolar lavage fluid. Fibroblasts under basal culture conditions express much higher levels of IL-6 and GM-CSF compared with AMs. Coculture of AMs and alveolar type II cells, or coculture of AMs and lung fibroblasts, in contact cultures or Transwell chambers, revealed no synergistic effect. Therefore, such interaction does not explain the effects seen in vivo. Identification of the intercellular communication in vivo is still unresolved. However, fibroblasts appear to be an important source of inflammatory mediators in the lung. Key words: alveolar macrophages, alveolar type II cells, cytokines, fibroblasts, gene expression, lung, silica.