Molecular immunological analysis of early resistance existed in susceptible mice to protozoan infection.

为了了解中性粒细胞在利什曼原虫感染中的免疫调节作用，我们检测了感染耐药C3H/HeJ和易感BALB/c小鼠的中性粒细胞中细胞因子和/或趋化因子mrna的表达。我们还研究了中性粒细胞耗竭对腹膜巨噬细胞和引流淋巴结细胞表达细胞因子mrna的影响，以及对这些小鼠脚垫病变和寄生虫负担的影响。来自耐药C3H/HeJ而非易感BALB/c小鼠的中性粒细胞表达IL-12p40、IFN-1γ、TNF-α和一种由IFN-γ (MIG)诱导的Th1细胞趋化因子的mrna。中性粒细胞耗竭降低了耐药小鼠腹腔巨噬细胞中IFN-γ和TNF-α mrna的表达，但不影响引流淋巴结中IL-12p40 mrna的表达和足垫病变的生长。另一方面，BALB/c易感小鼠的中性粒细胞缺失不影响TNF-α和Th2细胞趋化因子单核细胞衍生趋化因子（MDC）在腹膜巨噬细胞中的表达，但诱导引流淋巴结细胞IL-4 mRNA的早期表达，加重足垫病变，增加寄生虫负担。我们的研究结果表明，即使在易感的BALB/c中，而在C3H/HeJ小鼠中，在感染早期也需要中性粒细胞产生一定的抗性。

To understand the immunomodulatory roles of neutrophils in Leishmania major infection, we examined-the expression of cytokine and/or chemokine mRNAs from neutrophils of the infected resistant C3H/HeJ and susceptible BALB/c mice. We also examined the effects of neutrophil depletion on the expression of cytokine mRNAs by peritoneal macrophages and draining lymph nodes cells and on the footpad lesions and parasite burdens in these mice. Neutrophils from resistant C3H/HeJ but not from susceptible BALB/c mice expressed mRNAs for IL-12p40, IFN-1γ, TNF-α, and a Th1 cell chemoattractive chemokine, monikine induced by IFN-γ (MIG). Neutrophil depletion of the resistant mice reduced the expression of IFN-γ and TNF-α mRNAs in peritoneal macrophages, but did not affected the expression of IL-12p40 mRNAs in draining lymph nodes and the growth of footpad lesions. On the other hand, neutrophil depletion of susceptible BALB/c mice did not affect the expression of TNF-α and a Th2 cell chemoattractive chemokine, monocyte derived chemokine (MDC) in peritoneal macrophages, but induced the early stage expression of IL-4 mRNA in draining lymph nodes cells and exacerbated the footpad lesions and increased the parasite burden. Our results suggest that even in susceptible BALB/c but not in C3H/HeJ mice there is a certain resistance requiring neutrophils at the early stage of infection.