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We were interested in identifying mechanisms linking IFN signaling to negative host responses against <jats:italic>L. monocytogenes<\/jats:italic> infection. Herein, we found that infection of myeloid cells with <jats:italic>L. monocytogenes<\/jats:italic> led to a coordinated induction of type I IFNs and activation of the integrated stress response (ISR). Infected cells did not induce <jats:italic>Xbp1<\/jats:italic> splicing or BiP upregulation, indicating that the unfolded protein response was not triggered. CHOP (<jats:italic>Ddit3<\/jats:italic>) gene expression was upregulated during the ISR activation induced by <jats:italic>L. monocytogenes<\/jats:italic>. Myeloid cells deficient in either type I IFN signaling or PKR activation had less upregulation of CHOP following infection. CHOP\u2010deficient mice showed lower expression of innate immune cytokines and were more resistant than wild\u2010type counterparts following <jats:italic>L. monocytogenes<\/jats:italic> infection. These findings indicate that <jats:italic>L. monocytogenes<\/jats:italic> infection induces type I IFNs, which activate the ISR through PKR, which contributes to a detrimental outcome in the infected host.<\/jats:p>","DOI":"10.1002\/eji.201646856","type":"journal-article","created":{"date-parts":[[2017,3,7]],"date-time":"2017-03-07T14:29:13Z","timestamp":1488896953000},"page":"830-840","source":"Crossref","is-referenced-by-count":15,"title":["<i>Listeria monocytogenes<\/i> induces an interferon\u2010enhanced activation of the integrated stress response that is detrimental for resolution of infection in mice"],"prefix":"10.1002","volume":"47","author":[{"given":"Carolina","family":"Valderrama","sequence":"first","affiliation":[{"name":"Division of Immunobiology Department of Pathology and Immunology Washington University School of Medicine  St. Louis MO USA"},{"name":"Department of Microbiology, PhD Biomedical Sciences Program School of Medicine Universidad Nacional de Colombia  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