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These antibodies agglutinate bacteria and, even in sub-agglutinating conditions, inhibit\n                      <jats:italic toggle=\"yes\">V. cholerae<\/jats:italic>\n                      motility. To explore additional effects of OSP-specific antibodies, we examined the transcriptomic profiles of\n                      <jats:italic toggle=\"yes\">V. cholerae<\/jats:italic>\n                      exposed to a human anti-OSP monoclonal antibody in the presence of mucin, the main component of intestinal mucus, and the substance in which\n                      <jats:italic toggle=\"yes\">V. cholerae<\/jats:italic>\n                      and mucosal antibodies interact in infected humans. Beyond genes whose transcript levels were affected by either mucin alone or antibody alone, we identified a set of genes whose expression levels were specifically altered in the presence of both anti-OSP antibody and mucin. These genes are involved in diverse processes such as metabolism, transport, stress response, biofilm formation, motility, and second messenger signaling. Additional culture-based assays and a human small intestine enteroid model confirmed the broad impact of OSP-specific antibodies on\n                      <jats:italic toggle=\"yes\">V. cholerae<\/jats:italic>\n                      , including the inhibition of motility, downregulation of virulence mechanisms, and a shift of bacterial metabolism toward decreased synthesis of intermediates and precursors in a sessile state secreting extracellular matrix component of a biofilm. Collectively, our findings reveal that antibodies targeting\n                      <jats:italic toggle=\"yes\">V. cholerae<\/jats:italic>\n                      OSP markedly transform the pathogen\u2019s physiology and disrupt its virulence program. We propose that these effects explain how antibodies targeting\n                      <jats:italic toggle=\"yes\">V. cholerae<\/jats:italic>\n                      OSP mediate protection against cholera at the intestinal surface of infected humans.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Immunity to cholera is largely mediated by antibodies targeting the O-specific polysaccharide (OSP) of\n                        <jats:italic toggle=\"yes\">Vibrio cholerae,<\/jats:italic>\n                        including through agglutination as well as inhibition of bacterial motility. Here, we used bacterial transcriptomic, biochemical, and cellular analyses to evaluate additional effects of OSP-specific antibodies on\n                        <jats:italic toggle=\"yes\">V. cholerae<\/jats:italic>\n                        in complex media containing mucin and in a human enteroid-derived monolayer colonization model. We found that anti-OSP antibody in mucin impacts bacterial motility, growth, metabolic activity, extracellular matrix production, and levels of cyclic di-GMP. We did not observe a direct effect on bacterial viability, sodium motive force gradient, membrane integrity for large molecules, or virulence gene or regulon expression in bacterial cultures, although cholera toxin detection was significantly decreased in the enteroid model. Our results uncover the broad impact of anti-OSP antibodies in the presence of mucin on\n                        <jats:italic toggle=\"yes\">V. cholerae<\/jats:italic>\n                        physiology and suggest several ways OSP-specific antibodies mediate protection against cholera in humans.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.02235-25","type":"journal-article","created":{"date-parts":[[2025,9,12]],"date-time":"2025-09-12T11:51:21Z","timestamp":1757677881000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":1,"title":["Human antibody targeting\n                    <i>Vibrio cholerae<\/i>\n                    O1 O-specific polysaccharide induces an amotile hypovirulent bacterial phenotype: mechanism of protection against cholera"],"prefix":"10.1128","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3760-8090","authenticated-orcid":true,"given":"Smriti","family":"Verma","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/002pd6e78","id-type":"ROR","asserted-by":"publisher"}],"name":"Division of Infectious Diseases, Massachusetts General Hospital","place":["Boston, USA"]},{"id":[{"id":"https:\/\/ror.org\/002pd6e78","id-type":"ROR","asserted-by":"publisher"}],"name":"Division of Pediatric Gastroenterology and Nutrition, Mucosal Immunology and Biology Research Center, Massachusetts General Hospital","place":["Boston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Murat","family":"Cetinbas","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/002pd6e78","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Molecular Biology, Massachusetts General Hospital","place":["Boston, 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