生物谷报道：5月15日出版的《细胞—宿主与微生物》（Cell Host & Microbe）上刊载了一篇有关血红素加氧酶可促进疟原虫肝期感染的研究论文。
临床无症状的疟原虫肝期是形成疟疾感染和疾病的必经阶段。经研究发现血红素加氧酶-1（HO-1，由Hmox1编码）的表达在感染伯氏疟原虫及约氏疟原虫孢子的肝脏中呈上调趋势。
在肝脏中，HO-1的过度表达会引起寄生虫肝脏负荷成比例增加，每一个HO- 1的酶产物也会增加寄生虫肝脏负荷。反过来，缺乏Hmox1的小鼠能够彻底清除感染。在不含HO-1时，参与控制肝感染的各级炎性细胞因子增加。
这些结果表明，疟原虫肝期在刺激发炎的同时，也诱导HO-1的表达，而HO-1的表达可以调节宿主的炎症反应，保护受感染的肝细胞和促进感染肝期。（生物谷www.bioon.com）
生物谷推荐原始出处：
Cell Host & Microbe，Vol 3, 331-338, 15 May 2008，Sabrina Epiphanio, Maria M. Mota
Heme Oxygenase-1 Is an Anti-Inflammatory Host Factor that Promotes Murine Plasmodium Liver Infection
Sabrina Epiphanio,1,2 Sebastian A. Mikolajczak,3 Lígia A. Gonçalves,2 Ana Pamplona,1,2 Silvia Portugal,1,2 Sónia Albuquerque,1,2 Michael Goldberg,4 Sofia Rebelo,2 Daniel G. Anderson,5 Akin Akinc,6 Hans-Peter Vornlocher,7 Stefan H.I. Kappe,3 Miguel P. Soares,2 and Maria M. Mota1,2,
1 Unidade de Malária, Instituto de Medicina Molecular, Universidade de Lisboa, 1649-028 Lisboa, Portugal
2 Instituto Gulbenkian de Ciência, 2780-156 Oeiras, Portugal
3 Seattle Biomedical Research Institute, Seattle, WA 98109, USA
4 Department of Chemistry, Massachusetts Institute of Technology, Cambridge, MA 02139, USA
5 David H. Koch Institute for Integrative Cancer Research, Cambridge, MA 02139, USA
6 Alnylam Pharmaceuticals, 300 Third Street, Cambridge MA 02142, USA
7 Roche Kulmbach GmbH, Fritz-Hornschuch-Strasse 9, 95326 Kulmbach, Germany
Summary
The clinically silent Plasmodium liver stage is an obligatory step in the establishment of malaria infection and disease. We report here that expression of heme oxygenase-1 (HO-1, encoded by Hmox1) is upregulated in the liver following infection by Plasmodium berghei and Plasmodium yoelii sporozoites. HO-1 overexpression in the liver leads to a proportional increase in parasite liver load, and treatment of mice with carbon monoxide and with biliverdin, each an enzymatic product of HO-1, also increases parasite liver load. Conversely, mice lacking Hmox1 completely resolve the infection. In the absence of HO-1, the levels of inflammatory cytokines involved in the control of liver infection are increased. These findings suggest that, while stimulating inflammation, the liver stage of Plasmodium also induces HO-1 expression, which modulates the host inflammatory response, protecting the infected hepatocytes and promoting the liver stage of infection.
