CO-Opting the Host HO-1 Pathway in Tuberculosis and Malaria

Photini Sinnis; Joel D. Ernst

doi:10.1016/j.chom.2008.04.009

CO-Opting the Host HO-1 Pathway in Tuberculosis and Malaria

Photini Sinnis, Joel D. Ernst

Research output: Contribution to journal › Short survey › peer-review

6 Scopus citations

Abstract

Infection with Mycobacterium tuberculosis and Plasmodium species results in upregulation of the host heme oxygenase-1 pathway. In tuberculosis infection, this leads to upregulation of the bacterial "dormancy regulon," whereas in malaria, it enhances the efficiency with which sporozoites develop into exoerythrocytic stages. Here we discuss these findings as well as some of the interesting questions they raise.

Original language	English (US)
Pages (from-to)	277-279
Number of pages	3
Journal	Cell Host and Microbe
Volume	3
Issue number	5
DOIs	https://doi.org/10.1016/j.chom.2008.04.009
State	Published - May 15 2008
Externally published	Yes

ASJC Scopus subject areas

Parasitology
Microbiology
Virology

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10.1016/j.chom.2008.04.009

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title = "CO-Opting the Host HO-1 Pathway in Tuberculosis and Malaria",

abstract = "Infection with Mycobacterium tuberculosis and Plasmodium species results in upregulation of the host heme oxygenase-1 pathway. In tuberculosis infection, this leads to upregulation of the bacterial {"}dormancy regulon,{"} whereas in malaria, it enhances the efficiency with which sporozoites develop into exoerythrocytic stages. Here we discuss these findings as well as some of the interesting questions they raise.",

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N2 - Infection with Mycobacterium tuberculosis and Plasmodium species results in upregulation of the host heme oxygenase-1 pathway. In tuberculosis infection, this leads to upregulation of the bacterial "dormancy regulon," whereas in malaria, it enhances the efficiency with which sporozoites develop into exoerythrocytic stages. Here we discuss these findings as well as some of the interesting questions they raise.

AB - Infection with Mycobacterium tuberculosis and Plasmodium species results in upregulation of the host heme oxygenase-1 pathway. In tuberculosis infection, this leads to upregulation of the bacterial "dormancy regulon," whereas in malaria, it enhances the efficiency with which sporozoites develop into exoerythrocytic stages. Here we discuss these findings as well as some of the interesting questions they raise.

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JO - Cell Host and Microbe

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ER -

CO-Opting the Host HO-1 Pathway in Tuberculosis and Malaria

Abstract

ASJC Scopus subject areas

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