<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Nash ZM</submitter><funding>HHS | NIH | National Institute of General Medical Sciences</funding><funding>NIAID NIH HHS</funding><funding>HHS | NIH | National Institute of Allergy and Infectious Diseases</funding><pagination>e0063224</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11077949</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>15(5)</volume><pubmed_abstract>&lt;i>Bordetella&lt;/i> species that cause respiratory infections in mammals include &lt;i>B. pertussis&lt;/i>, which causes human whooping cough, and &lt;i>B. bronchiseptica&lt;/i>, which infects nearly all mammals. Both bacterial species produce filamentous hemagglutinin (FhaB) and adenylate cyclase toxin (ACT), prominent surface-associated and secreted virulence factors that contribute to persistence in the lower respiratory tract by inhibiting clearance by phagocytic cells. FhaB and ACT proteins interact with themselves, each other, and host cells. Using immunoblot analyses, we showed that ACT binds to FhaB on the bacterial surface before it can be detected in culture supernatants. We determined that SphB1, a surface protease identified based on its requirement for FhaB cleavage, is also required for AC</pubmed_abstract><journal>mBio</journal><pubmed_title>&lt;i>Bordetella&lt;/i> filamentous hemagglutinin and adenylate cyclase toxin interactions on the bacterial surface are consistent with FhaB-mediated delivery of ACT to phagocytic cells.</pubmed_title><pmcid>PMC11077949</pmcid><funding_grant_id>AI153160, AI129541</funding_grant_id><funding_grant_id>AI1007151</funding_grant_id><funding_grant_id>R01 AI094991</funding_grant_id><funding_grant_id>R01 AI153160</funding_grant_id><funding_grant_id>AI094991</funding_grant_id><funding_grant_id>R01 AI129541</funding_grant_id><pubmed_authors>Inatsuka CS</pubmed_authors><pubmed_authors>Nash ZM</pubmed_authors><pubmed_authors>Cotter PA</pubmed_authors><pubmed_authors>Johnson RM</pubmed_authors></additional><is_claimable>false</is_claimable><name>&lt;i>Bordetella&lt;/i> filamentous hemagglutinin and adenylate cyclase toxin interactions on the bacterial surface are consistent with FhaB-mediated delivery of ACT to phagocytic cells.</name><description>&lt;i>Bordetella&lt;/i> species that cause respiratory infections in mammals include &lt;i>B. pertussis&lt;/i>, which causes human whooping cough, and &lt;i>B. bronchiseptica&lt;/i>, which infects nearly all mammals. Both bacterial species produce filamentous hemagglutinin (FhaB) and adenylate cyclase toxin (ACT), prominent surface-associated and secreted virulence factors that contribute to persistence in the lower respiratory tract by inhibiting clearance by phagocytic cells. FhaB and ACT proteins interact with themselves, each other, and host cells. Using immunoblot analyses, we showed that ACT binds to FhaB on the bacterial surface before it can be detected in culture supernatants. We determined that SphB1, a surface protease identified based on its requirement for FhaB cleavage, is also required for AC</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 May</publication><modification>2026-06-02T08:32:40.005Z</modification><creation>2026-04-16T03:11:30.911Z</creation></dates><accession>S-EPMC11077949</accession><cross_references><pubmed>38534159</pubmed><doi>10.1128/mbio.00632-24</doi></cross_references></HashMap>