Micewithout HO-1 are more susceptible to bacterial sepsis when given exogenousheme before infection. However, the releaseof iron by HO-1 can benefit intracellular pathogens, such as Mycobacterium tuberculosis and Salmonellaenterica, by increasing iron availability.−,  Studies showthat mice treated with HO-1 inhibitors have decreased intra-macrophage M. tuberculosis burden and less pneumonic lesions,but increased serum interferon gamma (IFNγ) and lower transforminggrowth factor beta (TGF-β) levels. The gene discussed is HMOX1; the disease is infection.