Department of Genetics, University of Alabama at Birmingham, Birmingham, Alabama, USA.
FEMS Microbiol Lett. 2013 Jan;338(2):155-60. doi: 10.1111/1574-6968.12048. Epub 2012 Nov 28.
Few mycoplasmal polysaccharides have been described and little is known about their role in pathogenesis. The infection of mice with Mycoplasma pulmonis has been utilized in many in vivo and in vitro studies to gain a better understanding of host-pathogen interactions during chronic respiratory infection. Although alveolar macrophages have a primary role in host defence, M. pulmonis is killed inefficiently in vitro. One antiphagocytic factor produced by the mycoplasma is the family of phase- and size-variable Vsa lipoproteins. However, bacteria generally employ multiple strategies for combating host defences, with capsular polysaccharide often having a key role. We show here that mutants lacking the EPS-I polysaccharide of M. pulmonis exhibit increased susceptibility to binding and subsequent killing by alveolar macrophages. These results give further insight into how mycoplasmas are able to avoid the host immune system and sustain a chronic infection.
已描述了少数几种支原体多糖，但它们在发病机制中的作用知之甚少。用鼠型支原体感染小鼠已被广泛用于许多体内和体外研究，以更好地了解慢性呼吸道感染过程中宿主-病原体的相互作用。尽管肺泡巨噬细胞在宿主防御中起主要作用，但支原体在体外的杀伤效率很低。支原体产生的一种抗吞噬因子是相和大小可变的 Vsa 脂蛋白家族。然而，细菌通常采用多种策略来对抗宿主防御，其中荚膜多糖通常起着关键作用。我们在这里表明，缺乏鼠型支原体 EPS-I 多糖的突变体对肺泡巨噬细胞的结合和随后的杀伤作用更加敏感。这些结果进一步深入了解支原体如何能够逃避宿主免疫系统并维持慢性感染。
