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The Proceedings of the American Thoracic Society 4:240-246 (2007)
© 2007 The American Thoracic Society
doi: 10.1513/pats.200701-023AW
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Ozone and Pulmonary Innate Immunity

John W. Hollingsworth1, Steven R. Kleeberger2 and W. Michael Foster1

1 Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, Durham, North Carolina; and 2 National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina

Correspondence and requests for reprints should be addressed to John W. Hollingsworth, M.D., Division of Pulmonary, Allergy, and Critical Care Medicine, Duke University Medical Center, Box 3136, Durham, NC 27710. E-mail: holli017{at}mc.duke.edu

ABSTRACT

Ambient ozone (O3) is a commonly encountered environmental air pollutant with considerable impact on public health. Many other inhaled environmental toxicants can substantially affect pulmonary immune responses. Therefore, it is of considerable interest to better understand the complex interaction between environmental airway irritants and immunologically based human disease. The innate immune system represents the first line of defense against microbial pathogens. Intact innate immunity requires maintenance of an intact barrier to interface with the external environment, effective phagocytosis of microbial pathogens, and precise detection of pathogen-associated molecular patterns. We use ambient O3 as a model to highlight the importance of understanding the role of exposure to ubiquitous air toxins and regulation of basic immune function. Inhalation of O3 is associated with impaired antibacterial host defense, in part related to disruption of epithelial barrier and effective phagocytosis of pathogens. The functional response to ambient O3 seems to be dependent on many components of the innate immune signaling. In this article, we review the complex interaction between inhalation of O3 and pulmonary innate immunity.

Key Words: Toll-like receptor • tlr4 • environmental airways injury • macrophage • epithelia




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