Little is known about the host-parasite interactions that support successful chronic infection
and maintenance of the adult O. viverrini liver fluke in the human biliary tree. Despite the
anti-fluke immunological responses (16), it is clear that O. viverrini, like other parasitic
helminths, has evolved the means to establish, survive and reproduce in the host for
extended periods of time. We speculate that this is possible only if the liver fluke exploits
permissive host factors for a productive infection. Although several liver specific markers
are upregulated due to liver fluke infection, little information is available on the host factors
that are utilized by these parasites (17–22). Employing infection of the Mta1−/− mouse (23)
as a model system, we have now identified a distinct contribution of MTA1 in establishing a
positive mammalian host/parasite interaction. Moreover, we found that MTA1 plays a
significant role in driving periductal fibrosis in the liver and is an essential host factor for
parasite survival. Earlier studies have established a central role of MTA1 in tumorigenesis
and inflammatory responses (24–29). Based on these findings, we hypothesize that helminth
parasites such as O. viverrini utilize the Mta1 host factor for a successful long-term
infection. The Mta1 gene product is a chromatin bound coregulator involved in
transcriptional regulation of genes associated with multiple cellular pathways (29–31). We
now propose that host MTA1 represents a common regulatory factor that is utilized by many
parasites for a successful infection. To test this hypothesis, we investigated the role of
MTA1 in Opisthorchis viverrini mediated infection using Mta1-null (Mta1−/−) and Mta1-
wildtype (Mta1+/+) mice as a model system with the expression of MTA1 in liver flukeinduced
cholangiocarcinoma
Little is known about the host-parasite interactions that support successful chronic infectionand maintenance of the adult O. viverrini liver fluke in the human biliary tree. Despite theanti-fluke immunological responses (16), it is clear that O. viverrini, like other parasitichelminths, has evolved the means to establish, survive and reproduce in the host forextended periods of time. We speculate that this is possible only if the liver fluke exploitspermissive host factors for a productive infection. Although several liver specific markersare upregulated due to liver fluke infection, little information is available on the host factorsthat are utilized by these parasites (17–22). Employing infection of the Mta1−/− mouse (23)as a model system, we have now identified a distinct contribution of MTA1 in establishing apositive mammalian host/parasite interaction. Moreover, we found that MTA1 plays asignificant role in driving periductal fibrosis in the liver and is an essential host factor forparasite survival. Earlier studies have established a central role of MTA1 in tumorigenesisand inflammatory responses (24–29). Based on these findings, we hypothesize that helminthparasites such as O. viverrini utilize the Mta1 host factor for a successful long-terminfection. The Mta1 gene product is a chromatin bound coregulator involved intranscriptional regulation of genes associated with multiple cellular pathways (29–31). Wenow propose that host MTA1 represents a common regulatory factor that is utilized by manyparasites for a successful infection. To test this hypothesis, we investigated the role ofMTA1 in Opisthorchis viverrini mediated infection using Mta1-null (Mta1−/−) and Mta1-wildtype (Mta1+/+) mice as a model system with the expression of MTA1 in liver flukeinducedcholangiocarcinoma
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