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SP-A Preserves Airway Homeostasis During Mycoplasma pneumoniae Infection in Mice¹

Julie G. Ledford^*, Hisatsugu Goto^*, Erin N. Potts, Simone Degan, Hong Wei Chu, Dennis R. Voelker, Mary E. Sunday, George J. Cianciolo, William M. Foster, Monica Kraft and Jo Rae Wright^2,*

^* Department of Cell Biology, Department of Pulmonary, Allergy and Critical Care Medicine, and Department of Pathology, Duke University Medical Center, Durham, NC 27710; and Department of Medicine, National Jewish Medical Center, Denver, CO 80206

The lung is constantly challenged during normal breathing by a myriad of environmental irritants and infectious insults. Pulmonary host defense mechanisms maintain homeostasis between inhibition/clearance of pathogens and regulation of inflammatory responses that could injure the airway epithelium. One component of this defense mechanism, surfactant protein-A (SP-A), exerts multifunctional roles in mediating host responses to inflammatory and infectious agents. SP-A has a bacteriostatic effect on Mycoplasma pneumoniae (Mp), which occurs by binding surface disaturated phosphatidylglycerols. SP-A can also bind the Mp membrane protein, MPN372. In this study, we investigated the role of SP-A during acute phase pulmonary infection with Mp using mice deficient in SP-A. Biologic responses, inflammation, and cellular infiltration, were much greater in Mp infected SP-A^–/– mice than wild-type mice. Likewise, physiologic responses (airway hyperresponsiveness and lung compliance) to Mp infection were more severely affected in SP-A^–/– mice. Both Mp-induced biologic and physiologic changes were attenuated by pharmacologic inhibition of TNF-. Our findings demonstrate that SP-A is vital to preserving lung homeostasis and host defense to this clinically relevant strain of Mp by curtailing inflammatory cell recruitment and limiting an overzealous TNF- response.

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 The research in this work was supported by National Institutes of Health Grants F32HL091642, ES011961, PHL 073907, and HL084917.

² Address correspondence and reprint requests to Dr. Jo Rae Wright, Department of Cell Biology, Box 3709, Duke University Medical Center, Durham, NC 27710. E-mail address: j.wright{at}cellbio.duke.edu

³ Abbreviations used in this paper: SP, surfactant protein; Mp, Mycoplasma pneumoniae; BALF, bronchoalveolar lavage fluid; AHR, airway hyperresponsiveness; RT, resistance; BCA, bicinchoninic acid; PAS, Periodic acid-Schiff; WT, wild type; PPLO, pleuropneumonia-like organisms.