Valbuena Gustavo, Walker David H
Department of Pathology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-0609, USA.
Am J Trop Med Hyg. 2004 Oct;71(4):393-9.
Rickettsiae cause systemic infections such as Rocky Mountain spotted fever and boutonneuse fever. The main cellular target of these obligately intracellular bacteria is the endothelium. T lymphocytes are the most important effectors of immunity, and the CXCR3 ligands CXCL9 and CXCL10 may play an important role in the T cell-mediated clearance of rickettsiae from the infected vasculature as suggested by recent expression studies. Here we showed that antibody-mediated neutralization of CXCL9 and CXCL10, and CXCR3 gene knockout, had no effect on survival or bacterial loads of mice infected with rickettsiae. We also demonstrated that rickettsiae triggered the endothelial expression of intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 in vivo. These findings suggested that antigenic presentation by endothelial cells together with an endothelial inflammatory phenotype induced by the rickettsial infection may be sufficient to arrest T cells and trigger their anti-rickettsial effector mechanisms without the need for chemokines.
立克次氏体可引起全身性感染，如落基山斑疹热和纽扣热。这些专性细胞内细菌的主要细胞靶点是内皮细胞。T淋巴细胞是免疫的最重要效应细胞，最近的表达研究表明，CXCR3配体CXCL9和CXCL10可能在T细胞介导的从感染脉管系统清除立克次氏体中发挥重要作用。在此我们表明，抗体介导的CXCL9和CXCL10中和以及CXCR3基因敲除，对感染立克次氏体的小鼠的存活或细菌载量没有影响。我们还证明，立克次氏体在体内触发细胞间黏附分子1和血管细胞黏附分子1的内皮表达。这些发现表明，内皮细胞的抗原呈递以及立克次氏体感染诱导的内皮炎症表型可能足以捕获T细胞并触发其抗立克次氏体效应机制，而无需趋化因子。
