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Department of Internal Medicine, Justus-Liebig-University, Giessen, Germany
Surfactant protein A (SP-A) has been implicated in the regulation
of pulmonary host defense and inflammatory events. We analyzed the
impact of SP-A on the Candida albicans-induced cytokine
response in human alveolar macrophages (AM) and its precursor cells,
the monocytes, which rapidly expand the alveolar mononuclear phagocyte
pool under inflammatory conditions. Both recombinant human SP-A and
natural canine SP-A were employed. SP-A dose-dependently down-regulated
the proinflammatory cytokine response of AM and monocytes to both
viable and nonviable Candida, including TNF-
,
IL-1ß, macrophage inflammatory protein-1, and monocyte
chemoattractant protein-1. In contrast, SP-A did not affect the
baseline liberation of these cytokines. The release of the
antiinflammatory cytokines IL-1 receptor antagonist and IL-6 was not
inhibited by SP-A under baseline conditions and in response to fungal
challenge. The inhibitory effect of SP-A on proinflammatory cytokine
release was retained upon reassembly of the apoprotein with natural
surfactant lipids and in the presence of serum constituents, for
mimicry of plasma leakage into the alveolar space. It was not
reproduced by the homologous proteins complement component C1q and type
IV collagen. It was independent of Candida-SP-A binding
and phagocyte C1q receptor occupancy, but apparently demanded SP-A
internalization by the mononuclear phagocytes, effecting
down-regulation of proinflammatory cytokine synthesis at the
transcriptional level. We conclude that SP-A limits excessive
proinflammatory cytokine release in AM and monocytes confronted with
fungal challenge in the alveolar compartment. These data lend further
credit to an important physiological role of SP-A in regulating
alveolar host defense and inflammation.
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