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Although multiple virulence-associated factors have been identified, the mechanisms underlying meningitis development remain incompletely understood. In\n                      <jats:italic toggle=\"yes\">S. suis<\/jats:italic>\n                      , a\n                      <jats:italic toggle=\"yes\">srtBCD<\/jats:italic>\n                      pilus gene cluster has been identified; our previous study suggested its association with bacterial virulence. In this study, we investigated the role of the\n                      <jats:italic toggle=\"yes\">srtBCD<\/jats:italic>\n                      cluster in\n                      <jats:italic toggle=\"yes\">S. suis<\/jats:italic>\n                      pathogenesis and confirmed that SBP2\u2019 was specifically localized on the bacterial surface and was found to be essential for full virulence in a murine infection model, whereas deletion of other minor subunits had minimal impact. Using brain microvascular endothelial cells (BMECs), microglia, and a BALB\/c mouse model, we examined how SBP2\u2019 promotes the development of\n                      <jats:italic toggle=\"yes\">S. suis<\/jats:italic>\n                      meningitis. Our results show that SBP2\u2019 enhances bacterial colonization of BMECs and recruits host plasminogen, facilitating extracellular matrix (ECM) degradation, and thereby promoting bacterial invasion. In addition, SBP2\u2019 enables\n                      <jats:italic toggle=\"yes\">S. suis<\/jats:italic>\n                      to evade microglial phagocytosis and improves its intracellular survival. Importantly, a monoclonal antibody targeting SBP2\u2019 conferred significant immunoprotection in mice. Together, these findings identify SBP2\u2019 as an important virulence factor and plasminogen-binding receptor that facilitates\n                      <jats:italic toggle=\"yes\">S. suis<\/jats:italic>\n                      traversal of the blood-brain barrier.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        <jats:italic toggle=\"yes\">Streptococcus suis<\/jats:italic>\n                        is an important zoonotic bacterial pathogen that could lead to severe damage in the central nervous system, but the mechanism underlying the breakthrough of the blood-brain barrier is still unclear. Pili are commonly considered virulence factors and subunit vaccine candidates, but no pilus structure could be observed on the surface of\n                        <jats:italic toggle=\"yes\">S. suis<\/jats:italic>\n                        serotype 2. In this study, we found that the\n                        <jats:italic toggle=\"yes\">srtBCD<\/jats:italic>\n                        pilus cluster, which was considered a pseudogene because of the truncation of the major pilus subunit, could be expressed, and the truncated major pilus subunit could be detected on the cell surface and be involved in the pathogenesis of\n                        <jats:italic toggle=\"yes\">S. suis<\/jats:italic>\n                        serotype 2. Notably, monoclonal antibodies targeting SBP2\u2019 provide immunoprotection in mice, reducing bacterial loads and brain damage. These findings identify SBP2\u2019 as a key virulence factor and therapeutic target, offering insights into\n                        <jats:italic toggle=\"yes\">S. suis<\/jats:italic>\n                        meningitis mechanisms.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/aem.01267-26","type":"journal-article","created":{"date-parts":[[2026,8,10]],"date-time":"2026-08-10T13:00:51Z","timestamp":1786366851000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["The truncated major pilin subunit SBP2\u2019 contributes to\n                    <i>Streptococcus suis<\/i>\n                    meningitis by interacting with host 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