Sunnemark D, Frostegård J, Orn A, Harris R A
Microbiology and Tumorbiology Center MTC, Karolinska Institute, Stockholm, Sweden.
Scand J Immunol. 1998 Nov;48(5):480-4. doi: 10.1046/j.1365-3083.1998.00410.x.
Continuing our characterization of the immunopathological events occurring during experimental murine Chagas' disease, an immunohistological examination was conducted of the aortas of chronically infected CBA/J mice. Compared with non-infected mice of identical age, Trypanosoma cruzi-infected mice exhibited a marked vasculitis, with significant infiltration of inflammatory cells into the adventitial layer, including CD4+, CD8+ T cells and macrophages. Production of interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) was evident in the inflammatory infiltrate in the endothelial and smooth muscle layers. Vasculitis was most apparent in proximity to the heart, but extended along the aorta. Such an inflammation could lead to an alteration of the endothelium, altering the protective properties of this layer and further contributing to the focal pathology characteristic of this stage of infection.
为继续描述实验性小鼠恰加斯病期间发生的免疫病理事件，我们对慢性感染的CBA/J小鼠的主动脉进行了免疫组织学检查。与同龄未感染小鼠相比，感染克氏锥虫的小鼠表现出明显的血管炎，炎症细胞显著浸润到外膜层，包括CD4 +、CD8 + T细胞和巨噬细胞。在内皮和平滑肌层的炎症浸润中，白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）的产生明显。血管炎在心脏附近最为明显，但沿主动脉延伸。这种炎症可能导致内皮细胞改变，改变该层的保护特性，并进一步促成该感染阶段的局灶性病理特征。
