{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T22:26:35Z","timestamp":1789943195423,"version":"4.0.1"},"reference-count":33,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2014,6,3]],"date-time":"2014-06-03T00:00:00Z","timestamp":1401753600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["pathsocjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Pathology"],"published-print":{"date-parts":[[2014,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    <jats:italic>Streptococcus (S.) pneumoniae<\/jats:italic>\n                    is a common Gram\u2010positive pathogen in community\u2010acquired pneumonia and sepsis. Triggering receptor expressed on myeloid cells\u20101 (\n                    <jats:styled-content style=\"fixed-case\">TREM<\/jats:styled-content>\n                    \u20101) is a receptor on phagocytes known to amplify inflammatory responses. Previous studies showed that\n                    <jats:styled-content style=\"fixed-case\">TREM<\/jats:styled-content>\n                    \u20101 inhibition protects against lethality during experimental Gram\u2010negative sepsis. We here aimed to investigate the role of\n                    <jats:styled-content style=\"fixed-case\">TREM<\/jats:styled-content>\n                    \u20101 in an experimental model of pneumococcal pneumonia, using\n                    <jats:styled-content style=\"fixed-case\">TREM<\/jats:styled-content>\n                    \u20101\/3\u2010deficient (\n                    <jats:italic>\n                      Trem\u20101\/3\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    <\/jats:italic>\n                    ) and wild\u2010type (Wt) mice. Additionally\n                    <jats:italic>ex vivo<\/jats:italic>\n                    responsiveness of\n                    <jats:italic>\n                      Trem\u20101\/3\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    <\/jats:italic>\n                    neutrophils and macrophages was examined.\n                    <jats:italic>S. pneumoniae<\/jats:italic>\n                    infection resulted in a rapid recruitment of\n                    <jats:styled-content style=\"fixed-case\">TREM<\/jats:styled-content>\n                    \u20101\u2010positive neutrophils into the bronchoalveolar space, while high constitutive\n                    <jats:styled-content style=\"fixed-case\">TREM<\/jats:styled-content>\n                    \u20101 expression on alveolar macrophages remained unchanged.\n                    <jats:styled-content style=\"fixed-case\">TREM<\/jats:styled-content>\n                    \u20101\/3 deficiency led to increased lethality, accompanied by enhanced growth of\n                    <jats:italic>S. pneumoniae<\/jats:italic>\n                    at the primary site of infection and increased dissemination to distant organs. Within the first 3\u20136\u2009h of infection,\n                    <jats:italic>\n                      Trem\u20101\/3\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    <\/jats:italic>\n                    mice demonstrated a strongly impaired innate immune response in the airways, as reflected by reduced local release of cytokines and chemokines and a delayed influx of neutrophils.\n                    <jats:italic>\n                      Trem\u20101\/3\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    <\/jats:italic>\n                    alveolar macrophages produced fewer cytokines upon exposure to\n                    <jats:italic>S. pneumoniae in vitro<\/jats:italic>\n                    and were less capable of phagocytosing this pathogen.\n                    <jats:styled-content style=\"fixed-case\">TREM<\/jats:styled-content>\n                    \u20101\/3 deficiency did not influence neutrophil responsiveness to\n                    <jats:italic>S. pneumoniae<\/jats:italic>\n                    . These results identify\n                    <jats:styled-content style=\"fixed-case\">TREM<\/jats:styled-content>\n                    \u20101 as a key player in protective innate immunity during pneumococcal pneumonia, most likely by enhancing the early immune response of alveolar macrophages. Copyright \u00a9 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.\n                  <\/jats:p>","DOI":"10.1002\/path.4361","type":"journal-article","created":{"date-parts":[[2014,4,19]],"date-time":"2014-04-19T06:18:04Z","timestamp":1397888284000},"page":"357-367","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":52,"title":["Triggering receptor expressed on myeloid cells\u20101 (\n                    <scp>TREM<\/scp>\n                    \u20101) improves host defence in pneumococcal pneumonia"],"prefix":"10.1002","volume":"233","author":[{"given":"Tijmen J","family":"Hommes","sequence":"first","affiliation":[{"name":"Center for Experimental and Molecular Medicine, Academic Medical Centre University of Amsterdam  The Netherlands"},{"name":"Centre for Infection and Immunity, Academic Medical Centre University of Amsterdam  The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arie J","family":"Hoogendijk","sequence":"additional","affiliation":[{"name":"Center for Experimental and Molecular Medicine, Academic Medical Centre University of Amsterdam  The Netherlands"},{"name":"Centre for Infection and Immunity, Academic Medical Centre University of Amsterdam  The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark C","family":"Dessing","sequence":"additional","affiliation":[{"name":"Department of Pathology, Academic Medical Centre University of Amsterdam  The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cornelis","family":"van't Veer","sequence":"additional","affiliation":[{"name":"Center for Experimental and Molecular Medicine, Academic Medical Centre University of Amsterdam  The Netherlands"},{"name":"Centre for Infection and Immunity, Academic Medical Centre University of Amsterdam  The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandrine","family":"Florquin","sequence":"additional","affiliation":[{"name":"Department of Pathology, Academic Medical Centre University of Amsterdam  The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marco","family":"Colonna","sequence":"additional","affiliation":[{"name":"Department of Pathology Washington University in St. Louis  MO USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alex F","family":"de Vos","sequence":"additional","affiliation":[{"name":"Center for Experimental and Molecular Medicine, Academic Medical Centre University of Amsterdam  The Netherlands"},{"name":"Centre for Infection and Immunity, Academic Medical Centre University of Amsterdam  The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tom","family":"van der Poll","sequence":"additional","affiliation":[{"name":"Center for Experimental and Molecular Medicine, Academic Medical Centre University of Amsterdam  The Netherlands"},{"name":"Centre for Infection and Immunity, Academic Medical Centre University of Amsterdam  The Netherlands"},{"name":"Division of Infectious Diseases, Academic Medical Centre University of Amsterdam  The 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