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Mediators of Inflammation
Volume 2012 (2012), Article ID 140937, 6 pages
Review Article

Macrophage-Mediated Inflammation and Disease: A Focus on the Lung

1MRC Centre for Inflammation Research, Queen’s Medical Research Institute, University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ, UK
2Manchester Collaborative Centre for Inflammation Research (MCCIR), University of Manchester, Manchester M13 9PL, UK

Received 17 September 2012; Accepted 30 October 2012

Academic Editor: I-Ming Jou

Copyright © 2012 Emily Gwyer Findlay and Tracy Hussell. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The lung is exposed to a vast array of inhaled antigens, particulate matter, and pollution. Cells present in the airways must therefore be maintained in a generally suppressive phenotype so that excessive responses to nonserious irritants do not occur; these result in bystander damage to lung architecture, influx of immune cells to the airways, and consequent impairment of gas exchange. To this end, the resident cells of the lung, which are predominantly macrophages, are kept in a dampened state. However, on occasion the suppression fails and these macrophages overreact to antigenic challenge, resulting in release of inflammatory mediators, induction of death of lung epithelial cells, deposition of extracellular matrix, and development of immunopathology. In this paper, we discuss the mechanisms behind this macrophage-mediated pathology, in the context of a number of inflammatory pulmonary disorders.