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Inhalation of Staphylococcus aureus Enterotoxin A Induces IFN- and CD8 T Cell-Dependent Airway and Interstitial Lung Pathology in Mice¹

Department of Immunology, University of Connecticut Health Center, Farmington, CT 06032

Staphylococcus aureus, a primary source of bacterial superantigen (SAg), is known to colonize the human respiratory tract and has been implicated in airway inflammation. Studies have documented a role for SAgs in respiratory disorders, such as nasal polyps, chronic obstructive pulmonary disease, chronic rhinosinusitis, and asthma. However, cellular and molecular mediators involved in SAg-mediated pulmonary disease have not been clearly identified. In this study, we investigated the effect of intranasal staphylococcal enterotoxin A (SEA) exposure on murine lung. The pathological features in the lung resulting from SEA exposure had characteristics of both obstructive and restrictive pulmonary disorders. There was also an increase in bronchoalveolar lavage protein concentration and cellularity following SEA challenge. Massive CD8⁺Vβ3⁺ T cell accumulation observed in the lung was dependent on CD4 T cell help, both for recruitment and for IFN- synthesis. The primary source of IFN- synthesis was CD8 T cells, and depletion of these cells abrogated disease. IFN- deficiency also prevented SEA-mediated disease, and this was by enhancing early recruitment of neutrophils as detected in the bronchoalveolar lavage. Thus, IFN- appeared to selectively aid the recruitment of T cells to the lungs while preventing the neutrophil accumulation. Therefore, our results show that IFN--producing CD8 T cells mediated pulmonary alveolitis and inflammation, which were dependent upon CD4 T cells for their recruitment to the lung.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grants AI 142858 and AI 52108 (to A.T.V.).

² Address correspondence and reprint requests to Dr. Anthony T. Vella, Department of Immunology, University of Connecticut Health Center, 263 Farmington Avenue, MC1319, Farmington, CT 06030. E-mail address: vella{at}uchc.edu

³ Abbreviations used in this paper: SAg, superantigen; ARDS, acute respiratory distress syndrome; BAL, bronchoalveolar lavage; BCA, bicinchoninic acid; BSS, balanced salt solution; i.n., intranasal; LNs, lymph nodes; SEA, staphylococcal enterotoxin A; SEB, staphylococcal enterotoxin B; WT, wild type.

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