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Type 1 fimbria, the short hair-like appendage assembled on the bacterial surface, plays a pivotal role in adhesion and invasion in . The type III secretion system (T3SS), another bacterial surface appendage, facilitates 's replication by delivering effectors into host cells. Our previous research demonstrated that T3SS protein EseJ inhibits adhesion and invasion of by suppressing type 1 fimbria. However, how EseJ suppresses type 1 fimbria remains elusive. In this study, a -like operator (nt -245 to -1 of ) upstream of type 1 fimbrial operon in was identified, and EseJ inhibits type 1 fimbria through the -like operator. Moreover, through DNA pull-down and electrophoretic mobility shift assay, an AraC-type T3SS regulator, EsrC, was screened and verified to bind to nt -145 to -126 and nt -50 to -1 of , suppressing type 1 fimbria. EseJ is almost abolished upon the depletion of EsrC. EsrC and EseJ impede type 1 fimbria expression. Intriguingly, nutrition and microbiota-derived indole activate type 1 fimbria through downregulating T3SS, alleviating EsrC or EseJ's inhibitory effect on -like operator of type 1 fimbrial operon. By this study, it is revealed that upon entering the gastrointestinal tract, rich nutrients and indole downregulate T3SS and thereof upregulate type 1 fimbria, stimulating efficient adhesion and invasion; upon being internalized into epithelium, the limit in indole and nutrition switches on T3SS and thereof switches off type 1 fimbria, facilitating effector delivery to guarantee 's survival/replication .IMPORTANCEIn this work, we identified the -like operator of type 1 fimbrial operon in , which was suppressed by the repressors-T3SS protein EseJ and EsrC. We unveiled that upregulates type 1 fimbria upon sensing rich nutrition and the microbiota-derived indole, thereof promoting the adhesion of . The increase of indole and nutrition promotes type 1 fimbria by downregulating T3SS. The decrease in EseJ and EsrC alleviates their suppression on type 1 fimbria, and .
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http://dx.doi.org/10.1128/aem.00862-24 | DOI Listing |
Nature
September 2025
Department of Microbiology and Immunology, University of Illinois Chicago, Chicago, IL, USA.
Enteric pathogens engage in complex interactions with the host and the resident microbiota to establish gut colonization. Although mechanistic interactions between enteric pathogens and bacterial commensals have been extensively studied, whether and how commensal fungi affect enteric infections remain largely unknown. Here we show that colonization with the common human gut commensal fungus Candida albicans worsened infections with the enteric pathogen Salmonella enterica subsp.
View Article and Find Full Text PDFNat Commun
September 2025
Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD, Australia.
Carbapenem-resistant Enterobacterales pose a critical global health threat, exemplified by increasing resistance of uropathogenic E. coli (UPEC) that cause urinary tract infections (UTIs). Here, we investigate the publicly available EnteroBase dataset and identify a signal of increasing UTI caused by phylogroup A E.
View Article and Find Full Text PDFVet Microbiol
October 2025
Department of Preventive Veterinary Medicine, College of Veterinary Medicine, Shandong Agricultural University, Taian 271017, China; Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Taian 271017, China; Shandong Provincial Engineering Technology Research
Salmonella biofilm (BF) formation is crucial for persistent infections, with fimbrial adhesion being key. The regulatory role of the lpfD gene, encoding the tip adhesin of long polar fimbriae (LPF), in BF development is not well understood. This study used whole-genome sequencing to identify the lpfD gene difference between high-BF-forming strain DSE06 and low-BF-forming strain DSK01.
View Article and Find Full Text PDFJ Appl Microbiol
August 2025
Microbiology, Immunology and Parasitology Department, Institute of Basic Health Science, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
Aims: This study proposed an in-house in vitro model to investigate the effects of two prebiotic treatments on the gastrointestinal microbiota of piglets.
Methods And Results: The model involved suspending piglet feces in a culture medium to simulate the ileum and proximal colon regions of the swine gastrointestinal tract. The prebiotics tested were mannanoligosaccharides (MOS) and sodium butyrate.
Gut Pathog
August 2025
Department of Pediatrics, National Taiwan University Hospital, Taipei, Taiwan R.O.C..
Background: Symbiotic microbes benefit the host, but the emergence of pathobionts leads to disease. An invasive Escherichia coli LI60C3, isolated from mouse colonocytes, shows colitogenic and tumorigenic properties. Despite extensive research on the role of microbiota in colorectal cancer (CRC) development, the genetic markers associated with this pathobiont remain elusive.
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