{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,3]],"date-time":"2026-04-03T23:48:58Z","timestamp":1775260138675,"version":"3.50.1"},"reference-count":43,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2018,12,4]],"date-time":"2018-12-04T00:00:00Z","timestamp":1543881600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100008968","name":"National Research Council Sri Lanka","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["1R01AI101049\u201001"],"award-info":[{"award-number":["1R01AI101049\u201001"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["1R01AI101049\u201001"],"award-info":[{"award-number":["1R01AI101049\u201001"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["American J Rep Immunol"],"published-print":{"date-parts":[[2019,1]]},"abstract":"<jats:sec>\n                    <jats:title>Problem<\/jats:title>\n                    <jats:p>\n                      IFN\u2010alpha receptor deficiency (IFNAR\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      ) enhances immunity to\n                      <jats:italic>Listeria monocytogenes<\/jats:italic>\n                      (LM) and\n                      <jats:italic>Salmonella enterica<\/jats:italic>\n                      serovar Typhimurium (ST) in the non\u2010pregnant state by inhibiting pathogen\u2010induced immune cell death. However, the roles of IFNAR signaling in modulating immunity to infection during pregnancy are not well understood.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Method of Study<\/jats:title>\n                    <jats:p>\n                      C57BL\/6J wild\u2010type (WT) and IFNAR\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice were infected systemically with LM or ST. Bacterial burden in spleen and individual placentas was enumerated at day 3 post\u2010infection. Immune cell numbers and percentages were quantified in spleen and individual placentas, respectively, through flow cytometry. Cytokine expression in serum, spleen, and individual placentas was measured through cytometric bead array.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      IFNAR\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice exhibited decreased splenic monocyte numbers in non\u2010pregnant and pregnant state, and an altered distribution of placental immune cell types in the non\u2010infected state. IFNAR\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice controlled LM infection more effectively than WT mice even during pregnancy. This correlated with enhanced serum IL\u201012 expression, despite reduced splenic monocyte numbers relative to WT controls. In contrast, pregnant IFNAR\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice unlike their non\u2010pregnant counterparts exhibited increased susceptibility to ST infection, which was associated with decreased serum IL\u201012 expression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Type I IFN responses differentially impact host resistance to LM and ST infection during pregnancy through modulation of immune cell distribution and cytokine responses.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/aji.13068","type":"journal-article","created":{"date-parts":[[2018,10,30]],"date-time":"2018-10-30T12:09:16Z","timestamp":1540901356000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Type I interferons differentially modulate maternal host immunity to infection by\n                    <i>Listeria monocytogenes<\/i>\n                    and\n                    <i>Salmonella enterica<\/i>\n                    serovar Typhimurium during pregnancy"],"prefix":"10.1111","volume":"81","author":[{"given":"Gerard","family":"Agbayani","sequence":"first","affiliation":[{"name":"Department of Biochemistry, Microbiology and Immunology University of Ottawa Ottawa Ontario Canada"},{"name":"Division of Life Sciences, Human Health Therapeutics National Research Council Canada Ottawa Ontario Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kristina","family":"Wachholz","sequence":"additional","affiliation":[{"name":"Division of Life Sciences, Human Health Therapeutics National Research Council Canada Ottawa Ontario Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shawn P.","family":"Murphy","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynecology University 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