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Am J Physiol Lung Cell Mol Physiol 296: L1085-L1095, 2009. First published April 24, 2009; doi:10.1152/ajplung.90622.2008
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Intranasal organic dust exposure-induced airway adaptation response marked by persistent lung inflammation and pathology in mice

Jill A. Poole,1,2 Todd A. Wyatt,1,2 Peter J. Oldenburg,2 Margaret K. Elliott,2 William W. West,3 Joseph H. Sisson,2 Susanna G. Von Essen,2 and Debra J. Romberger1,2

1Omaha Veterans Affairs Medical Center; 2Pulmonary, Critical Care, Sleep, and Allergy Section, Department of Internal Medicine, and 3Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska

Submitted 15 December 2008 ; accepted in final form 9 April 2009

Organic dust exposure in agricultural environments results in an inflammatory response that attenuates over time, but repetitive exposures can result in chronic respiratory disease. Animal models to study these mechanisms are limited. This study investigated the effects of single vs. repetitive dust-induced airway inflammation in mice by intranasal exposure method. Mice were exposed to swine facility dust extract (DE) or saline once and once daily for 1 and 2 wk. Dust exposure resulted in increased bronchoalveolar lavage fluid neutrophils and macrophages after single and repetitive exposures. Lavage fluid TNF{alpha}, IL-6, keratinocyte chemoattractant, and macrophage inflammatory protein-2 were significantly increased after single and repetitive dust exposures, but were dampened in 2-wk dust-exposed mice compared with single exposure. Dust exposure induced PKC{alpha} and -{varepsilon} activation in isolated tracheal epithelial cells but were dampened with repetitive exposures. Ex vivo stimulation of alveolar macrophages from 2-wk animals demonstrated reduced cytokine responsiveness and phagocytic ability. Significant lung pathology occurred with development of mixed mononuclear cellular aggregates (T and B lymphocytes, phagocytes) after repetitive dust exposure, a novel observation. Airway hyperresponsiveness to methacholine occurred after single dust exposure but resolved after 2 wk. Collectively, intranasal exposure to DE results in significant lung inflammatory and pathological responses marked by a modulated innate immune response to single and repetitive dust exposures that is associated with PKC activity.

antigen presenting cell; phagocytosis; cytokines; aggregate; airway hyperresponsiveness


Address for reprint requests and other correspondence: J. A. Poole, Pulmonary, Critical Care, Sleep, and Allergy Section, Univ. of Nebraska Medical Center, 985300 The Nebraska Medical Center, Omaha, NE 68198-5300 (e-mail: japoole{at}unmc.edu)






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