송정민 (Cornell University) | 한빛사논문 > 한빛사

한빛사논문

조회132

Cornell University

CV File 527 kb

Sci. Adv., Jun 06 2025, 11 (23) eadt2040 | https://doi.org/10.1126/sciadv.adt2040 Molecular basis of the hepatobiliary tropism of typhoid toxin promoting Salmonella pathogenicity

Hwa Young Kim ¹, Gi Young Lee¹, Andrew J Thompson ², Ryan McBride ², Dah-Jiun Fu ³, James C Paulson ², Jeongmin Song ^{1 *}

¹Department of Microbiology and Immunology, Cornell University College of Veterinary Medicine, Ithaca, NY 14853, USA.
²Department of Molecular Medicine, The Scripps Research Institute, La Jolla, CA 92121, USA.
³Texas A&M Veterinary Medical Diagnostic Laboratory, College Station, TX 77843, USA.

^*Corresponding author: correspondence to Jeongmin Song

Abstract

Salmonella Typhi assembles and secretes two forms of typhoid toxin by using two receptor-binding subunits, PltB and PltC. Unlike PltB typhoid toxin, little is known about the tropism and functional consequences of PltC typhoid toxin. Here, we report that PltC typhoid toxin has hepatobiliary tropism through the binding of PltC subunit to sulfated glycans on liver sinusoidal endothelial cells and gallbladder epithelial cells. Critical bacterial and mammalian cell factors involved are PltC R109 residue and carbohydrate sulfotransferases CHST2/4. One notable effect associated with the hepatobiliary tropism of PltC typhoid toxin is a reduction in bile acids, consequently promoting S. Typhi pathogenicity in infected mice. Similarly, bile acids serve as anti-S. Typhi infectivity agents at the cellular level, as bile acids inhibit invasion of mammalian cells. These findings highlight a distinct mechanism used by a bacterial exotoxin promoting the pathogenicity of the cognate bacteria and offer insights into the development of antivirulence agents against PltC typhoid toxin and/or S. Typhi.

논문정보

형식Research article
게재일2025년 06월 (BRIC 등록일 2025-06-10)
연구진국외 연구진
분야 생명과학 > 감염생물학

댓글 작성 로그인

CV 열람하기

연락처 보기