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We found that protective immunity to a virulence factor of nasal mucosa-colonizing<jats:named-content content-type=\"genus-species\">Staphylococcus aureus<\/jats:named-content>, staphylococcal enterotoxin B (SEB), requires a functional NALT. We examined the role of NALT using intranasal (IN) vaccination with a recombinant SEB vaccine (rSEBv) combined with an adjuvant in a mouse model of SEB-induced toxic shock. The rSEBv was rapidly internalized by NALT cells at the mucosal barrier, and transport into NALT was accelerated by inclusion of a Toll-like receptor 4 (TLR4) agonist. Vaccine-induced germinal centers of B cells formed within NALT, accompanied by elevated levels of IgA<jats:sup>+<\/jats:sup>and IgG<jats:sup>+<\/jats:sup>cells, and these were further increased by TLR4 activation. The NALT was the site of specific anti-rSEBv IgA and IgG production but was also influenced by intraperitoneal (IP) inoculation and perhaps other isolated lymphoid follicles observed within the nasal cavity. Vaccination by the IN route generated robust levels of anti-rSEBv IgA in saliva, nasal secretions, and blood compared to much lower levels after IP vaccination. IN vaccination also induced secretion of anti-rSEBv IgG in the blood and nasal secretions. Significantly, the efficacy of IN vaccination was dependent on NALT, as surgical removal resulted in greater sensitivity to IN challenge with wild-type SEB. Thus, protective immunity to SEB within the nasal sinuses was elicited by responses originating in NALT.<\/jats:p>","DOI":"10.1128\/cvi.00477-10","type":"journal-article","created":{"date-parts":[[2011,2,17]],"date-time":"2011-02-17T03:35:31Z","timestamp":1297913731000},"page":"667-675","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":17,"title":["Nasal Immunity to Staphylococcal Toxic Shock Is Controlled by the Nasopharynx-Associated Lymphoid Tissue"],"prefix":"10.1128","volume":"18","author":[{"given":"Stefan","family":"Fernandez","sequence":"first","affiliation":[{"name":"United States Army Medical Research Institute of Infectious Diseases, 1425 Porter Street, Frederick, Maryland 21702"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emily D.","family":"Cisney","sequence":"additional","affiliation":[{"name":"United States Army Medical Research Institute of Infectious Diseases, 1425 Porter Street, Frederick, Maryland 21702"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shannan I.","family":"Hall","sequence":"additional","affiliation":[{"name":"United States Army Medical Research Institute of Infectious Diseases, 1425 Porter Street, Frederick, Maryland 21702"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert G.","family":"Ulrich","sequence":"additional","affiliation":[{"name":"United States Army Medical Research Institute of Infectious Diseases, 1425 Porter Street, Frederick, Maryland 21702"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1177\/09680519060120050701"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-1759(96)00243-8"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.76.24.12596-12602.2002"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.0105-2896.2005.00299.x"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1196\/annals.1384.012"},{"key":"e_1_3_3_7_2","doi-asserted-by":"crossref","first-page":"2698","DOI":"10.4049\/jimmunol.129.6.2698","article-title":"Surface phenotype of Peyer's patch germinal center cells: implications for the role of germinal centers in B cell differentiation","volume":"129","author":"Butcher E. 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