SP-A preserves airway homeostasis during Mycoplasma pneumoniae infection in mice

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, Jo Rae Wright

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


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-α. 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-α response.

Original languageEnglish (US)
Pages (from-to)7818-7827
Number of pages10
JournalJournal of Immunology
Issue number12
StatePublished - Jun 15 2009

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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