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However,\n            <jats:italic>Yersinia<\/jats:italic>\n            virulence activities can elicit activation of inflammasomes, which lead to inflammatory cell death and cytokine release to contain infection.\n            <jats:italic>Yersinia<\/jats:italic>\n            activation and evasion of inflammasomes have been characterized in murine macrophages but remain poorly defined in human cells, particularly intestinal epithelial cells (IECs), a primary site of intestinal\n            <jats:italic>Yersinia<\/jats:italic>\n            infection. In contrast to murine macrophages, we find that in both human IECs and macrophages,\n            <jats:italic>Yersinia pseudotuberculosis<\/jats:italic>\n            T3SS effectors promote evasion of the caspase-4 inflammasome, which senses cytosolic lipopolysaccharide. The anti-phagocytic YopE and YopH, as well as the translocation regulator YopK, were collectively responsible for evading inflammasome activation, in part by inhibiting\n            <jats:italic>Yersinia<\/jats:italic>\n            internalization mediated by YadA and \u03b21-integrin signaling. These data provide insight into the mechanisms of\n            <jats:italic>Yersinia-<\/jats:italic>\n            mediated inflammasome activation and evasion in human cells and reveal species-specific differences underlying the regulation of inflammasome responses to\n            <jats:italic>Yersinia<\/jats:italic>\n            .\n          <\/jats:p>\n          <jats:sec>\n            <jats:title>IMPORTANCE<\/jats:title>\n            <jats:p>\n              <jats:italic>Yersinia<\/jats:italic>\n              are responsible for significant disease burden in humans, ranging from recurrent disease outbreaks (yersiniosis) to pandemics (\n              <jats:italic>Yersinia pestis<\/jats:italic>\n              plague). Together with rising antibiotic resistance rates, there is a critical need to better understand\n              <jats:italic>Yersinia<\/jats:italic>\n              pathogenesis and host immune mechanisms, as this information will aid in developing improved immunomodulatory therapeutics. Inflammasome responses in human cells are less studied relative to murine models of infection, though recent studies have uncovered key differences in inflammasome responses between mice and humans. Here, we dissect human intestinal epithelial cell and macrophage inflammasome responses to\n              <jats:italic>Yersinia pseudotuberculosis<\/jats:italic>\n              . Our findings provide insight into species- and cell type-specific differences in inflammasome responses to\n              <jats:italic>Yersinia<\/jats:italic>\n              .\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1128\/mbio.01310-23","type":"journal-article","created":{"date-parts":[[2023,8,24]],"date-time":"2023-08-24T13:00:22Z","timestamp":1692882022000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":11,"title":["<i>Yersinia<\/i>\n            deploys type III-secreted effectors to evade caspase-4 inflammasome activation in human cells"],"prefix":"10.1128","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7016-7947","authenticated-orcid":false,"given":"Jenna","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Microbiology, University of Pennsylvania, Perelman School of Medicine , Philadelphia, Pennsylvania, 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