Infection

Infection

Tick-born diseases, including ehrlichiosis, anaplasmosis, and babesiosis, are often associated with profound hematologic dysfunction. Using murine models of human monocytic ehrlichiosis (HME) we are investigating the cellular and molecular changes that occur to the hematopoietic system during stress-induced inflammation. Our studies have revealed an important role for interferon (IFN) gamma-signaling in the development of anemia. At the same time, IFN-gamma it is critical for the infection-induced production of myeloid cells, in particular monocytes.  The impact of type I interferons (alpha and beta) in the activation of hematopoietic responses is being investigated in a severe, lethal model of ehrlichiosis induced by infection with Ixodes ovatus ehrlichia (IOE). A rapid and complete loss of HSCs and MPPs is observed and depends on type I interferon signaling. Current studies are aimed at discerning the direct and indirect effects of type I interferons on HSC and progenitor cell function in shock-like disease.

In collaboration with other laboratories in the Department and at the New York State Department of Health, we are also exploring other infection models to better understand how clinically-relevant infections induce both protective and pathologic changes in hematopoiesis.

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