生物谷報道：5月15日出版的《細胞—宿主與微生物》（Cell Host & Microbe）上刊載了一篇有關(guān)血紅素加氧酶可促進瘧原蟲肝期感染的研究論文,。
臨床無癥狀的瘧原蟲肝期是形成瘧疾感染和疾病的必經(jīng)階段,。經(jīng)研究發(fā)現(xiàn)血紅素加氧酶-1（HO-1，由Hmox1編碼）的表達在感染伯氏瘧原蟲及約氏瘧原蟲孢子的肝臟中呈上調(diào)趨勢,。
在肝臟中,，HO-1的過度表達會引起寄生蟲肝臟負荷成比例增加，每一個HO- 1的酶產(chǎn)物也會增加寄生蟲肝臟負荷,。反過來,，缺乏Hmox1的小鼠能夠徹底清除感染。在不含HO-1時,，參與控制肝感染的各級炎性細胞因子增加,。
這些結(jié)果表明，瘧原蟲肝期在刺激發(fā)炎的同時,，也誘導(dǎo)HO-1的表達,，而HO-1的表達可以調(diào)節(jié)宿主的炎癥反應(yīng)，保護受感染的肝細胞和促進感染肝期,。（生物谷www.bioon.com）
生物谷推薦原始出處：
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.
