Increased expression and secretion of ICAM-1 during experimental infection with Trypanosoma cruzi
Increased expression and secretion of ICAM-1 during experimental infection with Trypanosoma cruzi
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DOI：
10.1046/j.1365-3024.1996.d01-95.x
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发表时间：
1996-05-01
影响因子：
2.2
通讯作者：
Rottenberg, ME
中科院分区：
文献类型：
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作者：
Laucella, S;Salcedo, R;Rottenberg, ME
在本研究中，我们表明，脾脏和心脏感染的BALB/c小鼠与毒性Tulahuen或低毒性CA-I株克氏锥虫，含有更高的ICAM-1转录比未感染的对照。心肌细胞ICAM-1表达在蛋白水平上也增加，如通过流式细胞术、ELISA和免疫组织化学所测量的。粘附受体不仅存在于炎性细胞上，也存在于T.克氏病毒感染的小鼠。ICAM-1表达在急性期高于慢性期，并与炎性白细胞密度呈正相关。在感染CA-I或Tulahuen寄生虫的急性期，在小鼠血清中检测到可溶性ICAM-1（s-ICAM-1）滴度升高。已显示细胞因子，包括IFN-γ、IL-1 α、IL-6和TNF-α，调节ICAM-1的表达。感染CA-1或Tulahuen菌株的小鼠的脾脏和心脏显示出这些细胞因子特异性mRNA的积累增加，在感染的急性期达到峰值。然而，在IFN-γ受体敲除（IFN-γ R（-））小鼠中，IFN-γ活性对于ICAM-1不是必需的。ICAM-1表达的上调可能是寄生虫感染的直接结果，因为其在不同谱系的细胞系上的密度在T.克鲁兹
In the present study we demonstrate that spleens and hearts from BALB/c mice infected with the virulent Tulahuen or the low virulent CA-I strains of Trypanosoma cruzi, contain substantially higher ICAM-1 transcripts than uninfected controls. ICAM-1 expression in heart cells was also increased at the protein level, as measured by flow cytometry, ELISA and immunohistochemistry. The adhesive receptor was observed not only on inflammatory cells but also on sarcolemma of cardiac myocytes from T. cruzi infected mice. ICAM-1 expression was higher during the acute phase than in the chronic phase of infection, and paralleled the density of inflammatory leukocytes. Elevated titres of soluble ICAM-1 (s-ICAM-1) were detected in sera from mice during the acute phase of infection with CA-I or Tulahuen parasites. Cytokines, including IFN-gamma, IL-1 alpha, IL-6 and TNA-alpha have been shown to modulate expression of ICAM-1. Spleens and hearts from mice infected with CA-1 or Tulahuen strains showed increased accumulation of mRNAs specific for these cytokines, which peaked during the acute phase of infection. However, IFN-gamma activity was not necessary for ICAM-1 in IFN-gamma receptor knock-out (IFN-gamma R(-)) mice. Upregulation of ICAM-1 expression might be a direct consequence of parasite infection, since its density on cell lines of different lineages was enhanced after 24 or 48 h of infection with T. cruzi.