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M\u03a6 play a crucial role in either terminating an infection at an early stage or succumbing to bacterial replication and colonization. However, our understanding of how\n                      <jats:italic toggle=\"yes\">Rickettsia<\/jats:italic>\n                      species invade host cells, including M\u03a6, remains poorly defined. In this study, we describe a mechanism of host invasion by\n                      <jats:italic toggle=\"yes\">Rickettsia<\/jats:italic>\n                      species, involving rickettsial phosphatidylserine (PS), as a ligand, and the CD300f receptor on M\u03a6. Our data reveal that engulfment of both pathogenic\n                      <jats:italic toggle=\"yes\">Rickettsia typhi<\/jats:italic>\n                      (the etiologic agent of murine typhus) and\n                      <jats:italic toggle=\"yes\">Rickettsia rickettsii<\/jats:italic>\n                      (the etiologic agent of Rocky Mountain spotted fever) species, as well as the non-pathogenic\n                      <jats:italic toggle=\"yes\">Rickettsia montanensis<\/jats:italic>\n                      , is significantly reduced in bone marrow-derived macrophages (BMDM\u03a6) from CD300f\n                      <jats:sup>-\/-<\/jats:sup>\n                      mice, as compared to that of wild-type (WT) animals. Furthermore, our mechanistic analysis suggests bacterial PS as the potential source for the CD300f-mediated rickettsiae engulfment by M\u03a6.\n                      <jats:italic toggle=\"yes\">In vivo<\/jats:italic>\n                      infection studies using WT and CD300f\n                      <jats:sup>-\/-<\/jats:sup>\n                      C57BL\/6J mice show that CD300f\n                      <jats:sup>-\/-<\/jats:sup>\n                      animals are protected against\n                      <jats:italic toggle=\"yes\">R. typhi<\/jats:italic>\n                      - or\n                      <jats:italic toggle=\"yes\">R. rickettsii<\/jats:italic>\n                      -induced fatal rickettsiosis, which corroborates with the level of the bacterial burden detected in the spleens of the mice. Adoptive transfer studies reveal that CD300f-expressing M\u03a6 are important mediators to control rickettsiosis\n                      <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                      . Collectively, our findings describe a previously unappreciated role for the efferocytic receptor, CD300f, to facilitate engulfment of rickettsiae within the host.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/iai.00059-25","type":"journal-article","created":{"date-parts":[[2025,5,1]],"date-time":"2025-05-01T10:08:52Z","timestamp":1746094132000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":1,"title":["Phosphatidylserine-binding receptor, CD300f, on macrophages mediates host invasion of pathogenic and non-pathogenic rickettsiae"],"prefix":"10.1128","volume":"93","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1436-2809","authenticated-orcid":true,"given":"Oliver H.","family":"Voss","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04rq5mt64","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine","place":["Baltimore, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Imran","family":"Moin","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04rq5mt64","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine","place":["Baltimore, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hodalis","family":"Gaytan","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04rq5mt64","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine","place":["Baltimore, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohammad","family":"Sadik","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04rq5mt64","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine","place":["Baltimore, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Saif","family":"Ullah","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/04rq5mt64","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine","place":["Baltimore, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9216-9270","authenticated-orcid":true,"given":"M. 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