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However,\n                    <jats:italic>S. suis<\/jats:italic>\n                    -induced BBB disruption has not been completely elucidated. In this study, we focused on the regulatory role of lysine acetyltransferase 2A (KAT2A) on BBB, which is a key regulator of cell death. We found that\n                    <jats:italic>S. suis<\/jats:italic>\n                    strain SC19 induces cell death in human cerebral microvascular endothelial cell line D3 (hCMEC\/D3) by membrane disruption and LDH release. During SC19 infection, KAT2A protein expression was markedly reduced but its mRNA expression was not affected. Further study demonstrated that SC19-induced KAT2A reduction was though ubiquitin\u2013proteasome-mediated protein degradation pathway. KAT2A inhibition using significantly exacerbated SC19-induced cell permeability disruption by transwell infection model. Consistently, KAT2A knockdown and pharmacological inhibition significantly aggravated SC19-induced downregulation of tight junction proteins including ZO-1 and occludin, whereas KAT2A overexpression partially restored their levels. Similarly, KAT2A inhibition aggravated SC19-induced downregulation of ZO-1 in mice brain and increased mice death rate, indicating the protective role of KAT2A on BBB. Mechanistically, KAT2A was found to regulate necroptosis in hCMEC\/D3. KAT2A knockdown aggravated necroptosis and upregulated phosphorylation of RIPK1, whereas RIPK1 inhibitor Nec-1 rescued SC19-induced necroptosis, indicating that KAT2A regulates RIPK1-dependent necroptosis during SC19 infection. Furthermore, quantitative proteomic analysis identified a network of putative KAT2A-mediated downstream targets and pathways that contribute to BBB integrity. Collectively, these findings reveal the underlying mechanism by which SC19 disrupts BBB through inducing KAT2A-mediated necroptosis and provide a potential therapeutic target for the treatment of bacterial meningitis.\n                  <\/jats:p>","DOI":"10.1186\/s13567-026-01736-8","type":"journal-article","created":{"date-parts":[[2026,3,25]],"date-time":"2026-03-25T13:17:57Z","timestamp":1774444677000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Streptococcus suis disrupts the blood\u2013brain barrier through inducing ubiquitin\u2013proteasome-mediated degradation of KAT2A"],"prefix":"10.1186","volume":"57","author":[{"given":"Yuqing","family":"Li","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hang","family":"Yin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tao","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shiqi","family":"Lang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tianning","family":"Yang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhiwei","family":"Li","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lianci","family":"Peng","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rendong","family":"Fang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2026,3,25]]},"reference":[{"key":"1736_CR1","doi-asserted-by":"publisher","first-page":"371","DOI":"10.2217\/fmb.10.2","volume":"5","author":"M Gottschalk","year":"2010","unstructured":"Gottschalk M, Xu J, Calzas C, Segura M (2010) Streptococcus suis: a new emerging or an old neglected zoonotic pathogen? 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