Wyler D J, Libby P, Prakash S, Prioli R P, Pereira M E
Division of Geographic Medicine and Infectious Diseases, New England Medical Center Hospitals, Boston, Massachusetts.
Infect Immun. 1987 Dec;55(12):3188-91. doi: 10.1128/iai.55.12.3188-3191.1987.
Myocardial fibrosis can occur as a complication of chronic infection of the heart with Trypanosoma cruzi (Chagas' disease) and can lead to serious disability. To assess whether there might be a direct relationship between intracellular parasitization and subsequent tissue fibrosis in this disease, we tested serum-free conditioned media from cultures of fibroblasts, vascular smooth-muscle cells, and myocardial cells for fibroblast-stimulating activity. Conditioned media from all infected cultures, but not from uninfected cultures, stimulated fibroblast [3H]thymidine incorporation, DNA and protein synthesis, and cell proliferation. Fibroblast-stimulating activity was also detected in extracts of amastigotes but not of trypomastigotes or epimastigotes. We conclude that parasitization of mesenchymal cells, including myocardial cells, results in elaboration of a fibroblast-stimulating factor(s), perhaps of parasite origin. We postulate that this factor may play a role in initiation of myocardial fibrosis in Chagas' disease.
心肌纤维化可作为克氏锥虫慢性心脏感染(恰加斯病)的并发症出现,并可导致严重残疾。为评估在该疾病中细胞内寄生与随后的组织纤维化之间是否可能存在直接关系,我们检测了成纤维细胞、血管平滑肌细胞和心肌细胞培养物的无血清条件培养基的成纤维细胞刺激活性。所有受感染培养物的条件培养基可刺激成纤维细胞[3H]胸苷掺入、DNA和蛋白质合成以及细胞增殖,而未受感染培养物的条件培养基则无此作用。在无鞭毛体提取物中也检测到了成纤维细胞刺激活性,但在锥鞭毛体或上鞭毛体提取物中未检测到。我们得出结论,包括心肌细胞在内的间充质细胞的寄生会导致一种可能源自寄生虫的成纤维细胞刺激因子的产生。我们推测该因子可能在恰加斯病心肌纤维化的起始过程中起作用。