ArticleInfection and immunity2009
Establishment of systemic Brucella melitensis infection through the digestive tract requires urease, the type IV secretion system, and lipopolysaccharide O antigen.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
56 citing papers in PubMed.
- Spatiotemporal dynamics of multi-organ pathology and antigen localization in BALB/c mice following intragastric infection withFrontiers in cellular and infection microbiology · 2026Article
- OralFrontiers in microbiology · 2026Article
- Tuft-cell-derived IL-25 regulates intestinal ILC2 in response toFrontiers in immunology · 2026Article
- Brucella abortus interferes with the inflammatory response and tissue repair in mice.Scientific reports · 2025Article
- Review on Current Research on Biosynthesis of Biosurfactants and the Regulation Influenced by Metal Ions.Journal of microbiology and biotechnology · 2025Review
- Enhanced Isolation ofMicroorganisms · 2025Article
- Combination ofFrontiers in microbiology · 2024Article
- Touching Base with Some Mediterranean Diseases of Interest from Paradigmatic Cases at the "Magna Graecia" University Unit of Infectious Diseases: A Didascalic Review.Diagnostics (Basel, Switzerland) · 2023Review
- Cell and Tissue Tropism of Brucella spp.Infection and immunity · 2023Review
- Activation of mucosal immunity as a novel therapeutic strategy for combating brucellosis.Frontiers in microbiology · 2022Review
- Article
- Live mucosal vaccination stimulates potent protectionFrontiers in immunology · 2022Article
- Quantification ofProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Protective efficacy of attenuatedJournal of veterinary science · 2021Article
- Uncovering the Hidden Credentials ofMicrobiology and molecular biology reviews : MMBR · 2021Review
- NLRP6-associated host microbiota composition impacts in the intestinal barrier to systemic dissemination of Brucella abortus.PLoS neglected tropical diseases · 2021Article
- Adhesive Functions or Pseudogenization of Type Va Autotransporters inFrontiers in cellular and infection microbiology · 2021Article
- Canine Brucellosis: An Update.Frontiers in veterinary science · 2021Review
- Idiosyncratic Biogenesis of Intracellular Pathogens-Containing Vacuoles.Frontiers in cellular and infection microbiology · 2021Review
- The Role of Neutrophils in Brucellosis.Microbiology and molecular biology reviews : MMBR · 2020Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Human brucellosis is caused mainly by Brucella melitensis, which is often acquired by ingesting contaminated goat or sheep milk and cheese. Bacterial factors required for food-borne infection of humans by B. melitensis are poorly understood. In this study, a mouse model of oral infection was characterized to assess the roles of urease, the VirB type IV secretion system, and lipopolysaccharide for establishing infection through the digestive tract. B. melitensis strain 16M was consistently recovered from the mesenteric lymph node (MLN), spleen, and liver beginning at 3 or 7 day postinfection (dpi). In the gut, persistence of the inoculum was observed up to 21 dpi. No inflammatory lesions were observed in the ileum or colon during infection. Mutant strains lacking the ureABC genes of the ure1 operon, virB2, or pmm encoding phosphomannomutase were constructed and compared to the wild-type strain for infectivity through the digestive tract. Mutants lacking the virB2 and pmm genes were attenuated in the spleen (P < 0.05) and MLN (P < 0.001), respectively. The wild-type and mutant strains had similar levels of resistance to low pH and 5 or 10% bile, suggesting that the reduced colonization of mutants was not the result of reduced resistance to acid pH or bile salts. In an in vitro lymphoepithelial cell (M-cell) model, B. melitensis transited rapidly through polarized enterocyte monolayers containing M-like cells; however, transit through monolayers containing only enterocytes was reduced or absent. These results indicate that B. melitensis is able to spread systemically from the digestive tract after infection, most likely through M cells of the mucosa-associated lymphoid tissue.
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