Alterations in macrophage functions by environmental chemicals.

Abstract

The establishment of infectious diseases is rarely entirely attributed to a single entity, but instead is the result of a primary stress and one or more secondary factors that interfere with homeostasis and the ability of the host to cope with the primary etiologic assault. Any environmental chemical that can suppress the normal functioning of the host's body defenses would be expected to increase the risk of the host to such diseases. Within the lung, the alveolar macrophages are the crucial elements responsible for defending the body against such airborne viable agents. The effects of inhaled gases and particulates on these defense cells are a major concern of the environmental health scientist since such chemicals have the capability of adversely affecting the integrity and functioning of these pulmonary defense cells. The objective of this report is to provide an overview that will improve our understanding of how a variety of environmental chemicals can alter the biochemical, physiological and immunological functioning of these cells.

Immunological Changes Produced in Rats by Prenatal Exposure to Carbon Monoxide

“…Macrophages provide a major defense against chemical injuries; dysfunction of macrophage can lead to indirect tissue damage through altered host resistance or to direct tissue injury. Environmental agents, especially particulates and gases (Gardner 1984), and to less extent lipophilic compounds (Luster & Blank 1987) can alter macrophage function. The cellular and molecular events of chemically-induced immunosuppression have not been so far elucidated.…”

Differential gene expression associated with inflammation in peripheral blood cells of patients with pneumoconiosis

“…The pathogenesis of silicosis and the role of alveolar macrophages in this process remain unclear 1) . Under normal circumstances, alveolar macrophages remove foreign substances and play a protective role 2 , 3) . Substantial evidence shows that long-term exposure to silica particles can cause macrophage apoptosis.…”

Phagocytized Silica Particles Cause IL-1β Release and Cell Death in Peritoneal Macrophages

“…Chronic exposure to respilable crystalline silica particles leads to silicosis, a potentially lethal disease that is marked by inflammation and fibrosis of the lung. Resident alveolar macrophages normally play a protective role in the lung by cleaning foreign materials [3,4]. However, scavenging of crystalline silica particles by the macrophages leads to direct release of inflammatory cytokines, which seems to be linked to development of silicosis [5,6].…”