{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T18:04:37Z","timestamp":1790705077159,"version":"4.1.0"},"reference-count":56,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2015,8,12]],"date-time":"2015-08-12T00:00:00Z","timestamp":1439337600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"},{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2015,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The capacity for intracellular survival within phagocytes is likely a critical factor facilitating the dissemination of\n            <jats:named-content content-type=\"genus-species\">Staphylococcus aureus<\/jats:named-content>\n            in the host. To date, the majority of work on\n            <jats:named-content content-type=\"genus-species\">S. aureus<\/jats:named-content>\n            -phagocyte interactions has focused on neutrophils and, to a lesser extent, macrophages, yet we understand little about the role played by dendritic cells (DCs) in the direct killing of this bacterium. Using bone marrow-derived DCs (BMDCs), we demonstrate for the first time that DCs can effectively kill\n            <jats:named-content content-type=\"genus-species\">S. aureus<\/jats:named-content>\n            but that certain strains of\n            <jats:named-content content-type=\"genus-species\">S. aureus<\/jats:named-content>\n            have the capacity to evade DC (and macrophage) killing by manipulation of autophagic pathways. Strains with high levels of Agr activity were capable of causing autophagosome accumulation, were not killed by BMDCs, and subsequently escaped from the phagocyte, exerting significant cytotoxic effects. Conversely, strains that exhibited low levels of Agr activity failed to accumulate autophagosomes and were killed by BMDCs. Inhibition of the autophagic pathway by treatment with 3-methyladenine restored the bactericidal effects of BMDCs. Using an\n            <jats:italic>in vivo<\/jats:italic>\n            model of systemic infection, we demonstrated that the ability of\n            <jats:named-content content-type=\"genus-species\">S. aureus<\/jats:named-content>\n            strains to evade phagocytic cell killing and to survive temporarily within phagocytes correlated with persistence in the periphery and that this effect is critically Agr dependent. Taken together, our data suggest that strains of\n            <jats:named-content content-type=\"genus-species\">S. aureus<\/jats:named-content>\n            exhibiting high levels of Agr activity are capable of blocking autophagic flux, leading to the accumulation of autophagosomes. Within these autophagosomes, the bacteria are protected from phagocytic killing, thus providing an intracellular survival niche within professional phagocytes, which ultimately facilitates dissemination.\n          <\/jats:p>","DOI":"10.1128\/iai.00358-15","type":"journal-article","created":{"date-parts":[[2015,6,23]],"date-time":"2015-06-23T01:31:23Z","timestamp":1435023083000},"page":"3445-3457","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":100,"title":["Manipulation of Autophagy in Phagocytes Facilitates Staphylococcus aureus Bloodstream Infection"],"prefix":"10.1128","volume":"83","author":[{"given":"Kate M.","family":"O'Keeffe","sequence":"first","affiliation":[{"name":"Host Pathogen Interactions Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mieszko M.","family":"Wilk","sequence":"additional","affiliation":[{"name":"Host Pathogen Interactions Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John M.","family":"Leech","sequence":"additional","affiliation":[{"name":"Host Pathogen Interactions Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alison G.","family":"Murphy","sequence":"additional","affiliation":[{"name":"Host Pathogen Interactions Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maisem","family":"Laabei","sequence":"additional","affiliation":[{"name":"Department of Biology and Biochemistry, University of Bath, Claverton Down, Bath, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ian R.","family":"Monk","sequence":"additional","affiliation":[{"name":"Microbiology Department, Moyne Institute of Preventative Medicine, Trinity College Dublin, Dublin, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruth C.","family":"Massey","sequence":"additional","affiliation":[{"name":"Department of Biology and Biochemistry, University of Bath, Claverton Down, Bath, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jodi A.","family":"Lindsay","sequence":"additional","affiliation":[{"name":"Institute for Infection and Immunity, St. George's, University of London, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Timothy J.","family":"Foster","sequence":"additional","affiliation":[{"name":"Microbiology Department, Moyne Institute of Preventative Medicine, Trinity College Dublin, Dublin, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joan A.","family":"Geoghegan","sequence":"additional","affiliation":[{"name":"Microbiology Department, Moyne Institute of Preventative Medicine, Trinity College Dublin, Dublin, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rachel M.","family":"McLoughlin","sequence":"additional","affiliation":[{"name":"Host Pathogen Interactions Group, School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2006.01.034"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.tim.2008.11.005"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0001409"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.175.6.3907"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.164.7.3713"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0005210"},{"key":"e_1_3_3_8_2","first-page":"71","article-title":"Entry of Mycobacterium tuberculosis into mononuclear phagocytes","volume":"215","author":"Schlesinger LS","year":"1996","unstructured":"Schlesinger LS. 1996. 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