Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, Florida, USA.
Infect Immun. 2013 Aug;81(8):3045-54. doi: 10.1128/IAI.00497-13. Epub 2013 Jun 10.
Chlamydia trachomatis is a Gram-negative obligate intracellular bacterium that preferentially infects epithelial cells. Professional phagocytes provide C. trachomatis only a limited ability to survive and are proficient killers of chlamydiae. We present evidence herein that identifies a novel host defense protein, perforin-2, that plays a significant role in the eradication of C. trachomatis during the infection of macrophages. Knockdown of perforin-2 in macrophages did not alter the invasion of host cells but did result in chlamydial growth that closely mirrored that detected in HeLa cells. C trachomatis L2, serovar B, and serovar D and C. muridarum were all equally susceptible to perforin-2-mediated killing. Interestingly, induction of perforin-2 expression in epithelial cells is blocked during productive chlamydial growth, thereby protecting chlamydiae from bactericidal attack. Ectopic expression of perforin-2 in HeLa cells, however, does result in killing. Overall, our data implicate a new innate resistance protein in the control of chlamydial infection and may help explain why the macrophage environment is hostile to chlamydial growth.
沙眼衣原体是一种革兰氏阴性专性细胞内细菌,优先感染上皮细胞。专业的吞噬细胞只能为沙眼衣原体提供有限的生存能力,并且是杀衣原体的高手。我们在此提出证据,确定了一种新型宿主防御蛋白——穿孔素-2,它在巨噬细胞感染期间对消除沙眼衣原体起着重要作用。在巨噬细胞中敲低穿孔素-2不会改变宿主细胞的入侵,但会导致类似于在 HeLa 细胞中检测到的衣原体生长。沙眼衣原体 L2、B 血清型和 D 血清型以及鼠衣原体都同样容易受到穿孔素-2介导的杀伤。有趣的是,在产毒沙眼衣原体生长过程中,上皮细胞中穿孔素-2的表达被抑制,从而保护衣原体免受杀菌攻击。然而,在 HeLa 细胞中异位表达穿孔素-2确实会导致杀伤。总的来说,我们的数据表明一种新的先天抵抗蛋白在控制衣原体感染方面发挥作用,这可能有助于解释为什么巨噬细胞环境对衣原体生长不利。