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Immunity from OMVs comes from immunoglobulin (Ig), particularly IgG, in the milk of mucosally immunized dams. Anti-OMV IgG renders<jats:named-content content-type=\"genus-species\">Vibrio cholerae<\/jats:named-content>organisms immotile, thus they pass through the small intestine without colonizing. However, the importance of motility inhibition for protection and the mechanism by which motility is inhibited remain unclear. By using both<jats:italic>in vitro<\/jats:italic>and<jats:italic>in vivo<\/jats:italic>experiments, we found that IgG inhibits motility by specifically binding to the O-antigen of<jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>. We demonstrate that the bivalent structure of IgG, although not required for binding to the O-antigen, is required for motility inhibition. Finally, we show using competition assays in suckling mice that inhibition of motility appears to be responsible for most, if not all, of the protection engendered by OMV vaccination, thus providing insight into the mechanism of immune protection.<\/jats:p>","DOI":"10.1128\/iai.00626-16","type":"journal-article","created":{"date-parts":[[2016,10,25]],"date-time":"2016-10-25T02:30:02Z","timestamp":1477362602000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":39,"title":["Immunity Provided by an Outer Membrane Vesicle Cholera Vaccine Is Due to O-Antigen-Specific Antibodies Inhibiting Bacterial Motility"],"prefix":"10.1128","volume":"85","author":[{"given":"Zhu","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Molecular Biology and Microbiology, Tufts University School of Medicine and Howard Hughes Medical Institute, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David W.","family":"Lazinski","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Microbiology, Tufts University School of Medicine and Howard Hughes Medical Institute, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew","family":"Camilli","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Microbiology, Tufts University School of Medicine and Howard Hughes Medical Institute, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.2471\/BLT.11.093427"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(12)60436-X"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1586\/erv.10.150"},{"key":"e_1_3_2_5_2","doi-asserted-by":"crossref","first-page":"264","DOI":"10.4049\/jimmunol.89.2.264","article-title":"Vibriocidal antibody inhibition (VAI) analysis: a technique for the identification of the predominant vibriocidal antibodies in serum and for the detection and identification of Vibrio cholerae antigens","volume":"89","author":"Finkelstein RA","year":"1962","unstructured":"Finkelstein RA . 1962. 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