Responses of Inflammatory Cells

ROBERT B. DEVLIN, ANDREW J. GHIO, and DANIEL L COSTA 

Environmental Protection Agency Research Triangle Park, North Carolina 

Anthropogenie dusts derived from combustion have been associated with inereased mortality and morbidity in numerous epidemiology studies. Despite these eonvineing assoeiations, toxieological and eonfrolled human exposure studies have not yet provided compelling evidenee pointing to a specific biological mechanism that may be responsible for increased mortality and morbidity. Fine 

Marcel Dekkbr, Inc. 270Madison Avenue New York, New York 10016 

The lack of any pliancy by the inflexible crystal surface of silica and asbestos predicts that placement of electrons into the symmetrically located coordination sites around iron will be incomplete. Complexed iron, with at least one free or labile coordination site, can subsequently mediate electron exchange via the 

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The very early peak of neutrophil invasion into an inflamed area is followed several hours later by a wave of a second class of phagocytic cells, the macrophages. This biphasic pattern of inflammatory cell movement and accumulation is observed in most acute inflammatory responses. The mononuclear phagocyte in the blood is known as the monocyte and differentiates... 

Corticosteroids are the most potent anti-inflammatory agents available for the treatment of asthma. The efficacy of corticosteroids is due to their ability to affect multiple inflammatory pathways, resulting in the suppression of inflammatory cell activation and function, prevention of microvascular leakage, decreased mucus production, and upregulation of P2-adrenergic receptors.10,18 Clinically, corticosteroids decrease airway inflammation, decrease AHR, decrease mucus production and secretion, and improve the response to P2-agonists.18 Corticosteroids for the treatment of asthma are available in inhaled, oral, and injectable dosage forms. 

Fig. 2. The role of MCP-1 (CCL2)/CCR2 in atherosclerosis is thought to occur through the response of endothelial cells and vascular smooth muscle cells to oxidized lipoproteins. After injury by oxidized lipoproteins, MCP-1 is released and attracts CCR2-expressing monocytes to the site of injury and activates them to secrete inflammatory mediators.

NiS04 and NiCl2 instilled into rat lungs also produced an inflammatory response (17). However, analysis of bronchoalveolar lavage fluid from rodents exposed to diesel exhaust containing 3.5 mg soot/m3, 7 h/day for 2, 12 or 17 days indicated no influx of inflammatory cells (20). Thus, the diesel soot, at lung burdens of 0.5 mg/g lung, does not produce an acute inflammatory response. 

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