Role of surfactant protein-A in nitric oxide production and mycoplasma killing in congenic C57BL/6 mice

Role of surfactant protein-A in nitric oxide production and mycoplasma killing in congenic C57BL/6 mice
复制标题

DOI:
10.1165/rcmb.2003-0246oc
复制
发表时间:
2004-03-01
影响因子:
6.4
通讯作者:
Matalon, S
Matalon, S
中科院分区:
医学1区
文献类型:
--
作者:
Hickman-Davis, JM;Gibbs-Erwin, J;Matalon, S

文献摘要

被引文献

相似文献

我们在支原体抗性 C57BL/6 背景 (B6.SP-A[-/-]) 上生成了同类表面活性剂蛋白 A (SP-A) 缺陷 (SP-A[-/-]) 小鼠,并与 C57BL/6 (136) 小鼠相比,表征了它们对支原体感染的反应。感染 10(6) 菌落形成单位 (cfu) 肺支原体的 B6.SP-A(-/-) 小鼠在感染后 72 小时 (p.i.) 的细菌肺负荷显着高于 B6 小鼠。在较高的感染剂量10(7)下,B6.SP-A(-/-)小鼠24小时肺cfu显着升高;然而,在注射后 48 小时和 72 小时,136 和 B6.SP-A(-/-) 小鼠之间的支原体 cfu 没有观察到差异。我们发现,与 B6.SP-A(-/-) 小鼠相比,未感染的 B6 小鼠支气管肺泡灌洗液中亚硝酸盐 (NO2_) 和硝酸盐 (NO3-) 水平较低。另一方面,与B6.SP-A(-/-)小鼠相比​​,用支原体感染B6小鼠导致支气管肺泡灌洗液NO2-和NO3-显着更高。这些数据表明 SP-A 可能有助于调节 NO 的产生以响应特定的刺激,即在没有细菌的情况下抑制 NO,在存在细菌的情况下增加 NO。这些数据表明,SP-A 对支原体杀灭的贡献可能仅限于较低剂量的病原体。
We generated congenic surfactant protein A (SP-A)-deficient (SP-A[-/-]) mice on the mycoplasma resistant C57BL/6 background (B6.SP-A[-/-]) and characterized their response to mycoplasma infection in comparison to C57BL/6 (136) mice. B6.SP-A(-/-) mice infected with 10(6) colony-forming units (cfu) of Mycoplasma pulmonis had significantly higher bacterial lung loads than B6 mice at 72 h postinfection (p.i.). At the higher infection dose of 10(7), B6.SP-A(-/-) mice had significantly higher lung cfu at 24 h; however, no difference in mycoplasma cfu was observed between 136 and B6.SP-A(-/-) mice at 48 and 72 h p.i. We found that uninfected B6 mice had lower bronchoalveolar lavage nitrite (NO2_) and nitrate (NO3-) levels as compared with B6.SP-A(-/-) mice. On the other hand, infection of B6 mice with mycoplasmas resulted in significantly higher bronchoalveolar lavage NO2- and NO3- as compared with B6.SP-A(-/-) mice. These data indicate that SP-A may help regulate NO production in response to a specific stimulus, i.e., suppression of NO in the absence of bacteria and increased NO in the presence of bacteria. These data indicate that the contribution of SP-A to mycoplasma killing may be limited to lower doses of pathogens.