硒能提高体液免疫、细胞免疫和非特异性免疫功能，显著提高吞噬细胞对病原微生物的杀菌活性，促进活性细胞因子和特异性抗体的产生，增强免疫活性物质的生物学效应。已经证明硒在预防乙型肝炎、SARS、艾滋病毒、禽流感等病毒性疾病中发挥重要作用。

近日，中国科学院动物研究所何宏轩研究员带领的野生动物疫病研究组在先前研究缺硒能够促进宿主对微小隐孢子虫感染的敏感性的基础上，又对细菌在宿主缺硒的条件下是否增强对宿主的损伤进行了研究探讨。研究表明，C57BL/6小鼠在缺硒的条件下，产单核李氏杆菌能够对宿主的先天性免疫反应造成损害，进而诱导宿主细胞因子在蛋白和mRNA水平上降低；在细胞水平上缺硒引起参与先天性免疫反应的免疫细胞快速动员和激活在一定程度上下降；就小鼠器官荷菌水平来看，缺硒小鼠的小肠、肝脏和淋巴结在24-72h内细菌繁殖数量明显加快，而且在72-120h肝脏和脑组织内细菌存在时间明显延长。所有这些结果表明了宿主在缺硒条件下先天性免疫反应受到一定程度的抑制，加剧了细菌对宿主损伤的后果。该工作得到国家科技部973和中国科学院知识创新项目的支持。

BMC Immunology 2009, 10:55doi:10.1186/1471-2172-10-55

Selenium deficiency impairs host innate immune response and induces susceptibility to Listeria monocytogenes infection

Chengmin Wang1,2 , Haijing Wang1 , Jing Luo1,2 , Yi Hu1 , Lei Wei1 , Mingxing Duan3  and Hongxuan He1

1  National Research Center for Wildlife Born Diseases, Key Laboratory of Animal Ecology and Conservation Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, PR China
2  The Graduate University of Chinese Academy of Science, Beijing 100049, PR China
3  State Key Laboratory of Biomembrane and Membrane Biotechnology, Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing 100084, PR China

Background
Susceptibility or resistance to infection with Listeria monocytogenes correlates with Selenium (Se) deficiency in response to infection.

Results
Se-deficient mouse models of listeriosis were used to study the innate immune response during the course of L. monocytogenes infection. Blood samples from mouse models were used for Se status. The concentration of MDA, SOD, GPx and CAT in blood has revealed that lower Se level exist in Se-deficient mice. Intestine, mesenteric lymph node, liver, spleen and brain from each mouse were to study the bacterial burden in organs. The analysis of cell types of spleen from Se-deficient mice revealed that the ability of the host to elicit a rapid recruitment and activation of systemic innate immune response to infection was to a certain extent compromised under conditions of Se deficiency. The cytokine levels in the serum and cytokine expression levels in the livers from Se-deficient mice revealed that the innate immune response of Se-deficient mice was impaired throughout the course of infection. These results suggest that innate immune response is altered by Se deficiency after infection with L. monocytogenes.

Conclusion
In conclusion, induced susceptibility of host resistance is associated with an impaired innate immune response following infection with L. monocytogenes in C57BL/6 Se-deficient mice.