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Abstract
The exoerythrocytic stage of Plasmodium infection is a critical window for prophylactic intervention. Using genome-wide dual RNA sequencing of flow-sorted infected and uninfected hepatoma cells we show that the human mucosal immunity gene, mucin-13 (MUC13), is strongly upregulated during Plasmodium exoerythrocytic hepatic-stage infection. We confirm MUC13 transcript increases in hepatoma cell lines and primary hepatocytes. In immunofluorescence assays, host MUC13 protein expression distinguishes infected cells from adjacent uninfected cells and shows similar colocalization with parasite biomarkers such as UIS4 and HSP70. We further show that localization patterns are species independent, marking both P. berghei and P. vivax infected cells, and that MUC13 can be used to identify compounds that inhibit parasite replication in hepatocytes. This data provides insights into host-parasite interactions in Plasmodium infection, and demonstrates that a component of host mucosal immunity is reprogrammed during the progression of infection.
Highlights
The exoerythrocytic stage of Plasmodium infection is a critical window for prophylactic intervention
To investigate host–pathogen interactions in Plasmodium exoerythrocytic stages, we conducted a dual RNA sequencing study, a strategy that has proven useful in identifying novel interactions in other intracellular parasitic organisms, including T. gondii and Leishmania major[23,24,25]
Samples were collected at time 0, 24 and 48 h postinfection, infected and uninfected cells were separated using fluorescence-activated cell sorting
Summary
The exoerythrocytic stage of Plasmodium infection is a critical window for prophylactic intervention. We further show that localization patterns are species independent, marking both P. berghei and P. vivax infected cells, and that MUC13 can be used to identify compounds that inhibit parasite replication in hepatocytes. This data provides insights into host-parasite interactions in Plasmodium infection, and demonstrates that a component of host mucosal immunity is reprogrammed during the progression of infection. The disease, caused by protozoan parasites of the genus Plasmodium, is transmitted when a female Anopheline mosquito takes a blood meal and injects infectious Plasmodium sporozoites These sporozoites (typically less than 100) migrate to the liver where they invade hepatocytes. It is known that multiple proteins, including ROP18 kinase[8,9] and GRA1510, are secreted into the host cell, altering host cell signal transduction and inflammation[11]
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