Hickman-Davis J M, Michalek S M, Gibbs-Erwin J, Lindsey J R
Department of Comparative Medicine, School of Medicine, University of Alabama at Birmingham, 35294-0019, USA.
Infect Immun. 1997 Jun;65(6):2278-82. doi: 10.1128/iai.65.6.2278-2282.1997.
Indirect evidence suggests that innate immune mechanisms involving alveolar macrophages (AMs) are of major importance in antimycoplasmal defense. We compared the effects of AM depletion on intrapulmonary killing of Mycoplasma pulmonis during the early phase of infection in mycoplasma-resistant C57BL/6NCr (C57BL) and mycoplasma-susceptible C3H/HeNCr (C3H) mice. More than 80% of AMs were depleted in both strains of mice by intratracheal insufflation of liposome-encapsulated dichloromethylene bisphosphonate (L-Cl2MBP), compared to no significant AM depletion in either strain following insufflation of liposome-encapsulated phosphate-buffered saline (L-PBS), PBS alone, or no treatment. AM-depleted (L-Cl2MBP) and control (L-PBS) mice were infected intranasally with 10(5) CFU of M. pulmonis UAB CT, and their lungs were quantitatively cultured to assess intrapulmonary killing at 0, 8, 12, and 48 h postinfection. AM depletion exacerbated the infection in C57BL mice by reducing killing of the organism to a level comparable to that in C3H mice without AM depletion. In contrast, AM depletion did not alter killing in C3H mice. These results directly identify the AM as the main effector cell in early pulmonary antimycoplasmal defense and suggest that differences in mycoplasmal killing by AMs may explain the resistance of C57BL mice and the susceptibility of C3H mice to mycoplasmal infection.
间接证据表明，涉及肺泡巨噬细胞（AMs）的先天性免疫机制在抗支原体防御中至关重要。我们比较了在支原体抗性C57BL/6NCr（C57BL）和支原体易感C3H/HeNCr（C3H）小鼠感染早期，AMs耗竭对肺内肺炎支原体杀灭的影响。通过气管内注入脂质体包裹的二氯亚甲基双膦酸盐（L-Cl2MBP），两种品系小鼠中超过80%的AMs被耗竭，相比之下，注入脂质体包裹的磷酸盐缓冲盐水（L-PBS）、单独的PBS或不进行处理后，两种品系小鼠的AMs均无明显耗竭。AMs耗竭组（L-Cl2MBP）和对照组（L-PBS）小鼠经鼻感染10(5) CFU的肺炎支原体UAB CT，对其肺部进行定量培养，以评估感染后0、8、12和48小时的肺内杀灭情况。AMs耗竭通过将病原体的杀灭降低到与未进行AMs耗竭的C3H小鼠相当的水平，从而加重了C57BL小鼠的感染。相反，AMs耗竭并未改变C3H小鼠的杀灭情况。这些结果直接确定AMs是早期肺部抗支原体防御的主要效应细胞，并表明AMs对支原体杀灭的差异可能解释了C57BL小鼠的抗性和C3H小鼠对支原体感染的易感性。
