Macrophages deficient for HO-1 function have been shown to restrict intracellular iron levels during infection with Salmonella and to enhance production of reactive oxygen species which promote NFκB-mediated activation of a proinflammatory immune response (e.g. TNFα, iNOS, p47phox) leading to reduced survival of Salmonella [43]. This evidence concerns the gene NCF1 and infection.