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Novel non-flagellated surface motility mediated by chemical signaling in Citrobacter rodentium.

ABSTRACT: Enterohemorrhagic (EHEC) and enteropathogenic Escherichia coli (EPEC) are human intestinal pathogens of clinical importance and their mechanism of pathogenicity is widely studied. However, both EHEC and EPEC poorly infect mice, whereas they do not develop important characteristics of the disease, hindering studies about mechanisms of virulence in vivo. Citrobacter rodentium exhibits high similarity of its genes with these human pathogens, including the island of pathogenicity Locus of Enterocyte Effacement (LEE). Therefore, C. rodentium becomes an alternative in vivo model for microorganisms that harbor LEE. The QseC directly regulates LEE as well as virulence mechanisms on these pathogens. Here, we report a novel surface motility in C. rodentium QseC-mediated in this non-flagellated bacterium. Moreover, we show norepinephrine and ethanolamine act as environmental signals in this movement. Hence, this study clarifies a novel role of the sensor QseC in completely unreported motility process of C. rodentium.

SUBMITTER: Melchior K

PROVIDER: S-EPMC6863189 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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Novel non-flagellated surface motility mediated by chemical signaling in Citrobacter rodentium.

Melchior Karine K Moreira Cristiano Gallina CG

Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] 20190827 4

Enterohemorrhagic (EHEC) and enteropathogenic Escherichia coli (EPEC) are human intestinal pathogens of clinical importance and their mechanism of pathogenicity is widely studied. However, both EHEC and EPEC poorly infect mice, whereas they do not develop important characteristics of the disease, hindering studies about mechanisms of virulence in vivo. Citrobacter rodentium exhibits high similarity of its genes with these human pathogens, including the island of pathogenicity Locus of Enterocyte ...[more]

PMID: 31456170

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Project description:The Gram-negative enteric bacterium Citrobacter rodentium is a natural mouse pathogen that has been extensively used as a surrogate model for studying the human pathogens enteropathogenic and enterohemorrhagic Escherichia coli. All three pathogens produce similar attaching and effacing (A/E) lesions in the intestinal epithelium. During infection, these bacteria employ surface structures called fimbriae to adhere and colonize the host intestinal epithelium. For C. rodentium, the roles of only a small number of its genome-carried fimbrial operons have been evaluated. Here, we report the identification of a novel C. rodentium colonization factor, called gut colonization fimbria (Gcf), which is encoded by a chaperone-usher fimbrial operon. A gcfA mutant shows a severe colonization defect within the first 10 days of infection. The gcf promoter is not active in C. rodentium under several in vitro growth conditions; however, it is readily expressed in a C. rodentium ?hns1 mutant lacking the closest ortholog of the Escherichia coli histone-like nucleoid structuring protein (H-NS) but not in mutants with deletion of the other four genes encoding H-NS homologs. H-NS binds to the regulatory region of gcf, further supporting its direct role as a repressor of the gcf promoter that starts transcription 158 bp upstream of the start codon of its first open reading frame. The gcf operon possesses interesting novel traits that open future opportunities to expand our knowledge of the structure, regulation, and function during infection of these important bacterial structures.Fimbriae are surface bacterial structures implicated in a variety of biological processes. Some have been shown to play a critical role during host colonization and thus in disease. Pathogenic bacteria possess the genetic information for an assortment of fimbriae, but their function and regulation and the interplay between them have not been studied in detail. This work provides new insights into the function and regulation of a novel fimbria called Gcf that is important for early establishment of a successful infection by C. rodentium in mice, despite being poorly expressed under in vitro growth conditions. This discovery offers an opportunity to better understand the individual role and the regulatory mechanisms controlling the expression of specific fimbrial operons that are critical during infection.

Project description:The gut microbiota plays a crucial role in susceptibility to enteric pathogens, including Citrobacter rodentium, a model extracellular mouse pathogen that colonizes the colonic mucosa. C. rodentium infection outcomes vary between mouse strains, with C57BL/6 and C3H/HeN mice clearing and succumbing to the infection, respectively. Kanamycin (Kan) treatment at the peak of C57BL/6 mouse infection with Kan-resistant C. rodentium resulted in relocalization of the pathogen from the colonic mucosa and cecum to solely the cecal luminal contents; cessation of the Kan treatment resulted in rapid clearance of the pathogen. We now show that in C3H/HeN mice, following Kan-induced displacement of C. rodentium to the cecum, the pathogen stably colonizes the cecal lumens of 65% of the mice in the absence of continued antibiotic treatment, a phenomenon that we term antibiotic-induced bacterial commensalization (AIBC). AIBC C. rodentium was well tolerated by the host, which showed few signs of inflammation; passaged AIBC C. rodentium robustly infected naive C3H/HeN mice, suggesting that the AIBC state is transient and did not select for genetically avirulent C. rodentium mutants. Following withdrawal of antibiotic treatment, 35% of C3H/HeN mice were able to prevent C. rodentium commensalization in the gut lumen. These mice presented a bloom of a commensal species, Citrobacter amalonaticus, which inhibited the growth of C. rodentium in vitro in a contact-dependent manner and the luminal growth of AIBC C. rodentium in vivo. Overall, our data suggest that commensal species can confer colonization resistance to closely related pathogenic species. IMPORTANCE Gut bacterial infections involve three-way interactions between virulence factors, the host immune responses, and the microbiome. While the microbiome erects colonization resistance barriers, pathogens employ virulence factors to overcome them. Treating mice infected with kanamycin-resistant Citrobacter rodentium with kanamycin caused displacement of the pathogen from the colonic mucosa to the cecal lumen. Following withdrawal of the kanamycin treatment, 65% of the mice were persistently colonized by C. rodentium, which seemed to downregulate virulence factor expression. In this model of luminal gut colonization, 35% of mice were refractory to stable C. rodentium colonization, suggesting that their microbiotas were able to confer colonization resistance. We identify a commensal bacterium of the Citrobacter genus, C. amalonaticus, which inhibits C. rodentium growth in vitro and in vivo. These results show that the line separating commensal and pathogenic lifestyles is thin and multifactorial and that commensals may play a major role in combating enteric infection.

Dataset Information

Novel non-flagellated surface motility mediated by chemical signaling in Citrobacter rodentium.

Publications

Novel non-flagellated surface motility mediated by chemical signaling in Citrobacter rodentium.

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