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Departments of 1 Comparative Medicine, 2 Anesthesiology, 3 Physiology and Biophysics, and 4 Pediatrics, Schools of Medicine and Dentistry, University of Alabama at Birmingham, Birmingham, Alabama 35294
Mycoplasma pneumoniae is a
leading cause of pneumonia and exacerbates other respiratory diseases
in humans. We investigated the potential role of surfactant protein
(SP) A in antimycoplasmal defense using alveolar
macrophages (AMs) from C57BL/6NCr (C57BL) mice, which are highly
resistant to infections of Mycoplasma
pulmonis. C57BL AMs, activated with interferon
(IFN)-
and incubated with SP-A (25 µg/ml) at 37°C, produced
significant amounts of nitric oxide (· NO; nitrate and
nitrite production = 1.1 µM · h
1 · 105
AMs1) and effected an 83% decrease in
mycoplasma colony-forming units (CFUs) by 6 h postinfection.
Preincubation of AMs with the inducible nitric oxide synthase inhibitor
NG-monomethyl-L-arginine abolished
· NO production and SP-A-mediated killing of mycoplasmas. No
decrease in CFUs was seen when IFN--activated macrophages were
infected with mycoplasmas in the absence of SP-A despite significant
· NO production (nitrate and nitrite production = 0.6 µM · h1 · 105
AMs1). These results demonstrate that SP-A mediates
killing of mycoplasmas by AMs, possibly through an
· NO-dependent mechanism.
nitric oxide; peroxynitrite; pulmonary defenses; Mycoplasma pulmonis; opsonophagocytosis
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