Epigenetic paradigms/exemplars of the macrophage: inflammasome axis in Leishmaniasis

The infectious paradigms have recently led to the recognition interplay of complex phenomenon underpinning disease diagnosis and prognosis. Evidently, parasitic infection studies are depicting converging trends of the epigenetic, environmental, and microbiome contributions, assisting pathogen-directed modulations of host biological system. The molecular details of epigenetic variations and memory, along with the multi-omics data at the interface of the host–pathogen level becomes strong indicator of immune cell plasticity, differentiation, and pathogen survival. Despite being one of the most important aspects of the disease’s etiopathology, the epigenetic regulation of host–pathogen interactions and evolutionary epigenetics have received little attention thus far. Recent evidence has focused on the growing need to link epigenetic and microbiome modulations on parasite phenotypic plasticity and pathogen-induced host phenotypic plasticity for designing futuristic therapeutic regimes. Leishmaniasis is a neglected tropical illness with varying degrees of disease severity that is linked to a trans-species and epigenetic heredity process, including the pathogen-induced host and strain-specific modulations. The review configures research findings aligning to the epigenetic epidemiology niche, involving co-evolutionary epigenetic inheritance and plasticity disease models. The epigenetic exemplars focus on the host–pathogen interactome expanse at the macrophage—inflammasome axis.