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Surfactant protein A mediates mycoplasmacidal activity of alveolar macrophages
J M Hickman-Davis1, J R Lindsey, S Zhu
1Department of Comparative Medicine, School of Medicine, University of Alabama at Birmingham 35294, USA.
Abstract:
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)-gamma and incubated with SP-A (25 micrograms/ml) at 37 degrees C, produced significant amounts of nitric oxide (.NO; nitrate and nitrite production = 1.1 microM.h-1.10(5) AMs-1) 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-gamma-activated macrophages were infected with mycoplasmas in the absence of SP-A despite significant .NO production (nitrate and nitrite production = 0.6 microM.h-1.10(5) AMs-1). These results demonstrate that SP-A mediates killing of mycoplasmas by AMs, possibly through an .NO-dependent mechanism.
Insights
Surfactant protein A enhances nitric oxide production in mouse macrophages, leading to significant killing of Mycoplasma bacteria. This indicates SP-A
Area of Science:
- Immunology
- Microbiology
- Pulmonary Medicine
Background:
- Mycoplasma pneumoniae is a primary cause of pneumonia and worsens other respiratory conditions.
- Surfactant protein A (SP-A) is crucial for lung immune defense.
- Alveolar macrophages (AMs) play a key role in clearing respiratory pathogens.
Purpose of the Study:
- To investigate the role of SP-A in the defense against Mycoplasma infections.
- To determine if SP-A enhances the antimycoplasmal activity of macrophages.
Main Methods:
- Utilized alveolar macrophages (AMs) from C57BL/6NCr mice, known for resistance to Mycoplasma pulmonis.
- Activated AMs with interferon-gamma (IFN-γ) and treated with SP-A.
- Measured nitric oxide (.NO) production and mycoplasma colony-forming units (CFUs).
- Employed an inducible nitric oxide synthase (iNOS) inhibitor (NG-monomethyl-L-arginine) to assess .NO dependency.
Main Results:
- SP-A treatment significantly increased .NO production in IFN-γ-activated AMs.
- SP-A mediated an 83% reduction in mycoplasma CFUs within 6 hours.
- Inhibition of .NO production abolished the SP-A-mediated killing of mycoplasmas.
- AMs without SP-A showed no significant CFU reduction despite .NO production.
Conclusions:
- Surfactant protein A plays a critical role in mediating the killing of mycoplasmas by alveolar macrophages.
- The antimycoplasmal effect of SP-A appears to be dependent on nitric oxide production.
- SP-A represents a potential therapeutic target for enhancing host defense against Mycoplasma infections.