Surfactant protein-A inhibits Mycoplasma-induced dendritic cell maturation through regulation of HMGB-1 cytokine activity

Julie G. Ledford, Bernice Lo, Michele M. Kislan, Joseph M. Thomas, Katherine Evans, Derek W. Cain, Monica Kraft, Kristi L. Williams, Jo Rae Wright

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

During pulmonary infections, a careful balance between activation of protective host defense mechanisms and potentially injurious inflammatory processes must be maintained. Surfactant protein A (SP-A) is an immune modulator that increases pathogen uptake and clearance by phagocytes while minimizing lung inflammation by limiting dendritic cell (DC) and T cell activation. Recent publications have shown that SP-A binds to and is bacteriostatic for Mycoplasma pneumoniae in vitro. In vivo, SP-A aids in maintenance of airway homeostasis during M. pneumoniae pulmonary infection by preventing an overzealous proinflammatory response mediated by TNF-α. Although SP-Awas shownto inhibit maturation of DC sinvitro, the consequence of DC/SP-A interactionsinvivo has not been elucidated. In this article, weshow that the absence of SP-A during M. pneumoniae infection leads to increased numbers of mature DCs in the lung and draining lymph nodes during the acute phase of infection and, consequently, increased numbers of activated T and B cells during the course of infection. The findings that glycyrrhizin, a specific inhibitor of extracellular high-mobility group box-1 (HMGB-1) abrogated this effect and that SP-A inhibits HMGB-1 release from immune cells suggest that SP-A inhibits M. pneumoniae-induced DC maturation by regulating HMGB-1 cytokine activity.

Original languageEnglish (US)
Pages (from-to)3884-3894
Number of pages11
JournalJournal of Immunology
Volume185
Issue number7
DOIs
StatePublished - Oct 1 2010
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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