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Gonococci associated with\n                    <jats:styled-content style=\"fixed-case\">DGI<\/jats:styled-content>\n                    mainly express the outer membrane protein\n                    <jats:styled-content style=\"fixed-case\">\n                      PorB\n                      <jats:sub>IA<\/jats:sub>\n                    <\/jats:styled-content>\n                    that binds to the scavenger receptor expressed on endothelial cells (\n                    <jats:styled-content style=\"fixed-case\">SREC<\/jats:styled-content>\n                    \u2010\n                    <jats:styled-content style=\"fixed-case\">I<\/jats:styled-content>\n                    ) and mediates bacterial uptake. We recently demonstrated that this interaction relies on intact membrane rafts that acquire\n                    <jats:styled-content style=\"fixed-case\">SREC<\/jats:styled-content>\n                    \u2010\n                    <jats:styled-content style=\"fixed-case\">I<\/jats:styled-content>\n                    upon attachment of gonococci and initiates the signalling cascade that finally leads to the uptake of gonococci in epithelial cells. In this study, we analysed the role of sphingomyelinases and their breakdown product ceramide. Gonococcal infection induced increased levels of ceramide that was enriched at bacterial attachment sites. Interestingly, neutral but not acid sphingomyelinase was mandatory for\n                    <jats:styled-content style=\"fixed-case\">\n                      PorB\n                      <jats:sub>IA<\/jats:sub>\n                    <\/jats:styled-content>\n                    \u2010mediated invasion into host cells. Neutral sphingomyelinase was required to recruit the\n                    <jats:styled-content style=\"fixed-case\">PI<\/jats:styled-content>\n                    3 kinase to caveolin and thereby activates the\n                    <jats:styled-content style=\"fixed-case\">PI<\/jats:styled-content>\n                    3 kinase\u2010dependent downstream signalling leading to bacterial uptake. Thus, this study elucidates the initial signalling processes of bacterial invasion during\n                    <jats:styled-content style=\"fixed-case\">DGI<\/jats:styled-content>\n                    and demonstrates a novel role for neutral sphingomyelinase in the course of bacterial infections.\n                  <\/jats:p>","DOI":"10.1111\/cmi.12361","type":"journal-article","created":{"date-parts":[[2014,9,16]],"date-time":"2014-09-16T06:07:19Z","timestamp":1410847639000},"page":"241-253","source":"Crossref","is-referenced-by-count":26,"title":["Neutral sphingomyelinase 2 is a key factor for\n                    <scp>P<\/scp>\n                    or\n                    <scp>B<\/scp>\n                    \u2010dependent invasion of\n                    <scp>\n                      <i>N<\/i>\n                    <\/scp>\n                    <i>eisseria 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