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 language | English (US) |
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Pages (from-to) | 3884-3894 |
Number of pages | 11 |
Journal | Journal of Immunology |
Volume | 185 |
Issue number | 7 |
DOIs | |
State | Published - Oct 1 2010 |
Externally published | Yes |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology