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Infection of macrophages by the intracellular protozoan  Leishmania  leads to down-regulation of a number of macrophage innate host defense mechanisms, thereby allowing parasite survival and replication. The underlying molecular mechanisms involved remain largely unknown. In this study, we assessed epigenetic changes in macrophage DNA methylation in response to infection with  L. donovani  as a possible mechanism for  Leishmania  driven deactivation of host defense. We quantified and detected genome-wide changes of cytosine methylation status in the macrophage genome resulting from  L. donovani  infection. A high confidence set of 443 CpG sites was identified with changes in methylation that correlated with live  L. donovani  infection. These epigenetic changes affected genes that play a critical role in host defense such as the JAK/STAT signaling pathway and the MAPK signaling pathway. These results provide strong support for a new paradigm in host-pathogen responses, where upon infection the pathogen induces epigenetic changes in the host cell genome resulting in downregulation of innate immunity thereby enabling pathogen survival and replication. We therefore propose a model whereby  Leishmania  induced epigenetic changes result in permanent down regulation of host defense mechanisms to protect intracellular replication and survival of parasitic cells.

Leishmania donovani Infection Causes Distinct Epigenetic DNA Methylation Changes in Host Macrophages