In Europe and the US alone, more than three million people live with HIV and 15 to 19% of the population is over 65-years old. Collectively, IFN-γ significantly inhibits pathogen-associated intracellular iron sequestration in macrophages and consequently retards the growth of intracellular bacterial pathogens by decreasing iron availability. monocytogenes bacilli bacterial infection greatly down-regulates ferroportin expression. Similarly, IFN-γ-activated macrophages express higher ferroportin levels than untreated controls even after infection with L. In contrast, IFN-γ significantly reduces hepcidin secretion in S. tuberculosis infections significantly induce iron sequestration in human macrophages. In this study, we show that IFN-γ regulates the expression of iron-related proteins hepcidin, ferroportin, and ferritin to induce iron export from macrophages. We hypothesize that IFN-γ decreases iron availability to intracellular pathogens consequently limiting replication in these cells. Interferon-gamma (IFN-γ) is a central cytokine in host defense against intracellular pathogens and has been shown to promote iron export in macrophages. Regardless of the intrinsic virulence differences among Listeria monocytogenes, Salmonella enterica and Mycobacterium tuberculosis, these intracellular pathogens share the ability to survive and persist inside the macrophage and other cells and thrive in iron rich environments. Salmonellosis and listeriosis together accounted for more than one third of foodborne illnesses in the United States and almost half the hospitalizations for gastrointestinal diseases in 2018 while tuberculosis afflicted over 10 million people worldwide causing almost 2 million deaths.

Hearts of iron 4 how to export