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Discovered in the context of viral infections, type I IFNs are now known to have myriad effects in infectious and autoimmune disease settings. Type I IFN signaling during bacterial infections is dependent on many factors including whether the infecting bacterium is intracellular or extracellular, as different signaling pathways are activated. As such, the repercussions of type I IFN induction can positively or negatively impact the disease outcome. This review focuses on type I IFN induction and downstream consequences during infection with the following intracellular bacteria:<jats:italic>Chlamydia trachomatis<\/jats:italic>,<jats:italic>Listeria monocytogenes<\/jats:italic>,<jats:italic>Mycobacterium tuberculosis<\/jats:italic>,<jats:italic>Salmonella enterica<\/jats:italic>serovar Typhimurium,<jats:italic>Francisella tularensis<\/jats:italic>,<jats:italic>Brucella abortus<\/jats:italic>,<jats:italic>Legionella pneumophila<\/jats:italic>, and<jats:italic>Coxiella burnetii<\/jats:italic>. Intracellular bacterial infections are unique because the bacteria must avoid, circumvent, and even co-opt microbial \u201csensing\u201d mechanisms in order to reside and replicate within a host cell. Furthermore, life inside a host cell makes intracellular bacteria more difficult to target with antibiotics. Because type I IFNs are important immune effectors, modulating this pathway may improve disease outcomes. 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