{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T03:15:04Z","timestamp":1792034104983,"version":"4.4.0"},"reference-count":44,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2024,12,11]],"date-time":"2024-12-11T00:00:00Z","timestamp":1733875200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell. Infect. Microbiol."],"abstract":"<jats:sec><jats:title>Introduction<\/jats:title><jats:p>Typhoid fever is an infectious disease primarily caused by <jats:italic>Salmonella enterica<\/jats:italic> sv. Typhi (<jats:italic>S.<\/jats:italic> Typhi), a bacterium that causes as many as 20 million infections and 600,000 deaths annually. Asymptomatic chronic carriers of S. Typhi play a major role in the transmission of typhoid fever, as they intermittently shed the bacteria and can unknowingly infect humans in close proximity. An estimated 90% of chronic carriers have gallstones; biofilm formation on gallstones is a primary factor in the establishment and maintenance of gallbladder carriage. CsgD is a central biofilm regulator in <jats:italic>Salmonella<\/jats:italic>, but the <jats:italic>S.<\/jats:italic> Typhi <jats:italic>csgD<\/jats:italic> gene has a mutation that introduces an early stop codon, resulting in a protein truncated by 8 amino acids at the C-terminus. In this study, we investigate the role of role of CsgD in <jats:italic>S.<\/jats:italic> Typhi. <\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We introduced a fully functional copy of the <jats:italic>csgD<\/jats:italic> gene from <jats:italic>S.<\/jats:italic> Typhimurium into <jats:italic>S.<\/jats:italic> Typhi under both a native and a constitutive promoter and tested for red, dry, and rough (Rdar) colony morphology, curli fimbriae, cellulose, and biofilm formation. <\/jats:p><\/jats:sec><jats:sec><jats:title>Results and discussion<\/jats:title><jats:p>We demonstrate that although CsgD-regulated curli and cellulose production were partially restored, the introduction of the <jats:italic>S.<\/jats:italic> Typhimurium <jats:italic>csgD<\/jats:italic> did not induce the Rdar colony morphology. Interestingly, we show that CsgD does not have a significant role in S. Typhi biofilm formation, as biofilm-forming capacities depend more on the isolate than the CsgD regulator. This data suggests the presence of an alternative biofilm regulatory process in this human-restricted pathogen. <\/jats:p><\/jats:sec>","DOI":"10.3389\/fcimb.2024.1478488","type":"journal-article","created":{"date-parts":[[2024,12,10]],"date-time":"2024-12-10T19:12:03Z","timestamp":1733857923000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":13,"title":["Functional role of the biofilm regulator CsgD in Salmonella enterica sv. 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