Inhibition of Ca2+ influx by surfactant in NR8383 alveolar macrophages
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Pulmonary surfactants reduce alveolar surface tension and alter inflammatory cell function. We studied the effects of surfactant preparations on Ca2+ influx regulated by protein kinase C (PKC) and mitogen-activated protein kinases (MAPK) and cytokine secretion in the alveolar macrophage (AM) cell line NR8383.
Fura-2-loaded AMs were stimulated with zymosan (200 μg/ml), 1,2-dioctanoyl-sn-glycerol (DOG, 20 μM) or C6-ceramide (C6C, 10 μM) in the presence of exogenous surfactants (beractant, calfactant or colfosceril) or surfactant phospholipid (dipalmitoyl phosphatidylcholine, DPPC), at 250 μg/ml phospholipid and changes in cytosolic free Ca 2+ (Δ[Ca2+]i) and cytokines were measured.
Zymosan-induced Δ[Ca2+]i (117 ± 5 nM) at 3 min was reduced (p <0.001) by beractant (50 ± 6 nM), colfosceril (61 ± 2 nM), calfactant (46 ± 5 nM), and DPPC (52 ± 5 nM). Beractant inhibited the Δ[Ca2+]i by PKC stimulation with DOG and all preparations reduced the MAPK-induced Ca2+ influx by C6C. Beractant and Ca2+ channel blocker SKF 96365 (10 μM) together abolished the zymosan-stimulated Δ[Ca2+]i. Zymosan-stimulated TNF-α and IL-1β secretion was also inhibited by surfactant pretreatment.
These results indicate that exogenous surfactant inhibits Ca2+ influx and cytokine secretion in zymosan-stimulated AMs. This anti-inflammatory activity may be through an interaction with downstream signaling elements or Ca2+ channels.
- Inhibition of Ca2+ influx by surfactant in NR8383 alveolar macrophages
Volume 57, Issue 10 , pp 489-496
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- SP Birkhäuser Verlag Basel
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- Alveolar macrophage
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- 1. Department of Pediatrics, University of Texas Health Science Center, 7703 Floyd Curl Drive, MSC 7812, San Antonio, TX, 78229-3900, USA
- 2. National Center for Research Resources, National Institutes of Health, 1 Democracy Plaza, Room 1064, 6701 Democracy Blvd., Bethesda, MD, 20892, USA