Abstract:
: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.
journal_name
Cell Host Microbejournal_title
Cell host & microbeauthors
Epiphanio S,Mikolajczak SA,Gonçalves LA,Pamplona A,Portugal S,Albuquerque S,Goldberg M,Rebelo S,Anderson DG,Akinc A,Vornlocher HP,Kappe SH,Soares MP,Mota MMdoi
10.1016/j.chom.2008.04.003subject
Has Abstractpub_date
2008-05-15 00:00:00pages
331-8issue
5eissn
1931-3128issn
1934-6069pii
S1931-3128(08)00121-2journal_volume
3pub_type
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