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Surfactant protein A inhibits alveolar macrophage cytokine production by CD14-independent pathway

Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710

Submitted 13 December 2002 ; accepted in final form 4 September 2003

The lung collectin surfactant protein A (SP-A) has both anti-inflammatory and prophagocytic activities. We and others previously showed that SP-A inhibits the macrophage production of tumor necrosis factor (TNF)- stimulated by the gram-negative bacterial component LPS. We propose that SP-A decreases the production of proinflammatory cytokines by alveolar macrophages via a CD14-independent mechanism. SP-A inhibited LPS-simulated TNF- production in rat and mouse macrophages in the presence and absence of serum (72% and 42% inhibition, respectively). In addition, SP-A inhibited LPS-induced mRNA levels for TNF-, IL-1, and IL-1 as well as NF-B DNA binding activity. SP-A also diminished ultrapure LPS-stimulated TNF- produced by wild-type and CD14-null mouse alveolar macrophages by 58% and 88%, respectively. Additionally, SP-A inhibited TNF- stimulated by PMA in both wild-type and TLR4-mutant macrophages. These data suggest that SP-A inhibits inflammatory cytokine production in a CD14-independent manner and also by mechanisms independent of the LPS signaling pathway.

inflammation; lipopolysaccharide

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