Antoniazi Simone, Price Helen P, Kropf Pascale, Freudenberg Marina A, Galanos Chris, Smith Deborah F, Müller Ingrid
Imperial College London, Faculty of Medicine, Department of Immunology, Norfolk Place, London W2 1PG, United Kingdom.
Infect Immun. 2004 Sep;72(9):5168-74. doi: 10.1128/IAI.72.9.5168-5174.2004.
We studied the expression of a subset of chemokines, including RANTES/CCL5, MIP-1alpha/CCL3, IP-10/CXCL10, and MCP-1/CCL2, in Toll-like receptor (TLR)-competent and -deficient mice after infection with Leishmania major. Chemokine expression at the site of infection (the footpad), in the draining lymph nodes and in the spleens of infected animals was determined by using two different methods of analysis. The results indicate that L. major infection causes overall upregulation of RANTES/CCL5, MIP-1alpha/CCL3, IP-10/CXCL10, and MCP-1/CCL2 in the footpads and lymph nodes, while expression of these chemokines is constitutive in the spleens of TLR4-competent mice (C57BL/10ScSn) and TLR4-deficient mice (C57BL10/ScN). Different patterns of expression were detected depending on the time postinfection, but there was little variation in the expression of these four chemokines in the presence or absence of TLR4.
我们研究了在感染硕大利什曼原虫后,趋化因子的一个子集(包括RANTES/CCL5、MIP-1α/CCL3、IP-10/CXCL10和MCP-1/CCL2)在Toll样受体(TLR)功能正常和缺陷小鼠中的表达情况。通过两种不同的分析方法确定了感染动物的感染部位(足垫)、引流淋巴结和脾脏中的趋化因子表达。结果表明,硕大利什曼原虫感染导致足垫和淋巴结中RANTES/CCL5、MIP-1α/CCL3、IP-10/CXCL10和MCP-1/CCL2总体上调,而这些趋化因子在TLR4功能正常的小鼠(C57BL/10ScSn)和TLR4缺陷的小鼠(C57BL10/ScN)脾脏中是组成性表达的。根据感染后的时间检测到不同的表达模式,但在有或没有TLR4的情况下,这四种趋化因子的表达几乎没有差异。