{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T00:15:31Z","timestamp":1792023331287,"version":"4.4.0"},"update-to":[{"DOI":"10.1371\/journal.ppat.1010912","type":"new_version","label":"New version","source":"publisher","updated":{"date-parts":[[2022,10,25]],"date-time":"2022-10-25T00:00:00Z","timestamp":1666656000000}}],"reference-count":52,"publisher":"Public Library of Science (PLoS)","issue":"10","license":[{"start":{"date-parts":[[2022,10,13]],"date-time":"2022-10-13T00:00:00Z","timestamp":1665619200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["32202805"],"award-info":[{"award-number":["32202805"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.plospathogens.org"],"crossmark-restriction":false},"short-container-title":["PLoS Pathog"],"abstract":"<jats:p><jats:italic>Glaesserella parasuis<\/jats:italic>(<jats:italic>G<\/jats:italic>.<jats:italic>parasuis<\/jats:italic>), the primary pathogen of Gl\u00e4sser\u2019s disease, colonizes the upper respiratory tract and can break through the epithelial barrier of the respiratory tract, leading to lung infection. However, the underlying mechanisms for this adverse effect remain unclear. The<jats:italic>G<\/jats:italic>.<jats:italic>parasuis<\/jats:italic>serotype 5 SQ strain (HPS5-SQ) infection decreased the integrity of piglets\u2019 lung Occludin and Claudin-1. Autophagy regulates the function of the epithelial barrier and tight junction proteins (TJs) expression. We tested the hypothesis that HPS5-SQ breaking through the porcine respiratory epithelial barrier was linked to autophagy and Claudin-1 degradation. When HPS5-SQ infected swine tracheal epithelial cells (STEC), autophagosomes encapsulated, and autolysosomes degraded oxidatively stressed mitochondria covered with Claudin-1. Furthermore, we found that autophagosomes encapsulating mitochondria resulted in cell membrane Claudin-1 being unable to be replenished after degradation and damaged the respiratory tract epithelial barrier. In conclusion,<jats:italic>G<\/jats:italic>.<jats:italic>parasuis<\/jats:italic>serotype 5 breaks through the porcine respiratory epithelial barrier by inducing autophagy and interrupting cell membrane Claudin-1 replenishment, clarifying the mechanism of the<jats:italic>G<\/jats:italic>.<jats:italic>parasuis<\/jats:italic>infection and providing a new potential target for drug design and vaccine development.<\/jats:p>","DOI":"10.1371\/journal.ppat.1010912","type":"journal-article","created":{"date-parts":[[2022,10,13]],"date-time":"2022-10-13T18:03:15Z","timestamp":1665684195000},"page":"e1010912","update-policy":"https:\/\/doi.org\/10.1371\/journal.ppat.corrections_policy","source":"Crossref","is-referenced-by-count":23,"title":["Glaesserella parasuis serotype 5 breaches the porcine respiratory epithelial barrier by inducing autophagy and blocking the cell membrane Claudin-1 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