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For example, macrophages may undergo regulated cell death, including RIPK3-dependent necroptosis, as a means of combatting intracellular bacterial pathogens. However, bacteria have evolved mechanisms to evade or exploit immune responses.\n            <jats:italic>Salmonella<\/jats:italic>\n            is an intracellular pathogen that avoids and manipulates immune detection within macrophages. We examined the contribution of RIPK3 to\n            <jats:italic>Salmonella<\/jats:italic>\n            -induced macrophage death. Our findings indicate that noninvasive\n            <jats:italic>Salmonella<\/jats:italic>\n            does not naturally induce necroptosis, but it does so when caspases are inhibited. Moreover, RIPK3 induction (following caspase inhibition) does not impact host survival following\n            <jats:italic>Salmonella<\/jats:italic>\n            systemic infection. Finally, our data show that RIPK3 induction results in recruitment of low-inflammatory myeloid cells, which was unexpected, as necroptosis is typically described as highly inflammatory. Collectively, these data improve our understanding of pathogen-macrophage interactions, including outcomes of regulated cell death during infection\n            <jats:italic>in vivo<\/jats:italic>\n            , and reveal a potential new role for RIPK3 in resolving inflammation.\n          <\/jats:p>","DOI":"10.1128\/mbio.02588-20","type":"journal-article","created":{"date-parts":[[2020,10,5]],"date-time":"2020-10-05T14:49:16Z","timestamp":1601909356000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":7,"title":["RIPK3-Dependent Recruitment of Low-Inflammatory Myeloid Cells Does Not Protect from Systemic\n            <i>Salmonella<\/i>\n            Infection"],"prefix":"10.1128","volume":"11","author":[{"given":"John","family":"Satkovich","sequence":"first","affiliation":[{"name":"Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, Virginia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher J.","family":"Anderson","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, Virginia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher B.","family":"Medina","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology, and Cancer Biology, University of Virginia School of Medicine, Charlottesville, Virginia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matteo","family":"Ottolini","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, Virginia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John R.","family":"Lukens","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Center for Brain 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