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We found that the \u0394\n            <jats:italic>gltT<\/jats:italic>\n            \u0394\n            <jats:italic>gltM<\/jats:italic>\n            invasion defect in assay medium (AM) was alleviated in AM without 10% fetal bovine serum (FBS) [AM(\u2212S)]. The alleviation disappeared again in AM(\u2212S) supplemented with 500 \u03bcM glutamate. Glutamate uptake by the \u0394\n            <jats:italic>gltT<\/jats:italic>\n            \u0394\n            <jats:italic>gltM<\/jats:italic>\n            mutant was less efficient than that by the wild-type strain, but only upon HBMEC infection. We also observed that both GltT-GltM-dependent invasion and accumulation of ezrin, a key membrane-cytoskeleton linker, were more pronounced when\n            <jats:named-content content-type=\"genus-species\">N. meningitidis<\/jats:named-content>\n            formed larger colonies on HBMEC under physiological glutamate conditions. These results suggested that GltT-GltM-dependent meningococcal internalization into HBMEC might be induced by the reduced environmental glutamate concentration upon infection. Furthermore, we found that the amount of glutathione within the \u0394\n            <jats:italic>gltT<\/jats:italic>\n            \u0394\n            <jats:italic>gltM<\/jats:italic>\n            mutant was much lower than that within the wild-type\n            <jats:named-content content-type=\"genus-species\">N. meningitidis<\/jats:named-content>\n            strain only upon HBMEC infection and was correlated with intracellular survival. Considering that the\n            <jats:sc>l<\/jats:sc>\n            -glutamate obtained via GltT-GltM is utilized as a nutrient in host cells,\n            <jats:sc>l<\/jats:sc>\n            -glutamate uptake via GltT-GltM plays multiple roles in\n            <jats:named-content content-type=\"genus-species\">N. meningitidis<\/jats:named-content>\n            internalization into HBMEC.\n          <\/jats:p>","DOI":"10.1128\/iai.00654-15","type":"journal-article","created":{"date-parts":[[2015,6,23]],"date-time":"2015-06-23T01:31:23Z","timestamp":1435023083000},"page":"3555-3567","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":10,"title":["Multiple Functions of Glutamate Uptake via Meningococcal GltT-GltM\n            <scp>l<\/scp>\n            -Glutamate ABC Transporter in Neisseria meningitidis Internalization into Human Brain Microvascular Endothelial Cells"],"prefix":"10.1128","volume":"83","author":[{"given":"Hideyuki","family":"Takahashi","sequence":"first","affiliation":[{"name":"Department of Bacteriology I, National Institute of Infectious Diseases, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tatsuo","family":"Yanagisawa","sequence":"additional","affiliation":[{"name":"RIKEN Structural Biology Laboratory, Tsurumi, Yokohama, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kwang Sik","family":"Kim","sequence":"additional","affiliation":[{"name":"Division of Pediatric Infectious Diseases, Department of Pediatrics, School of Medicine, Johns Hopkins University, Baltimore, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shigeyuki","family":"Yokoyama","sequence":"additional","affiliation":[{"name":"RIKEN Structural Biology Laboratory, Tsurumi, Yokohama, 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