ArticleThe American journal of pathology2008
Shiga toxin-mediated disease in MyD88-deficient mice infected with Escherichia coli O157:H7.
Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 54 citations in OpenAlex.
- Lactic Acid Bacteria with Probiotic Potential Regulating Macrophages: Mechanisms, Regulatory Features, and Clinical Applications.Probiotics and antimicrobial proteins · 2026Review
- Monocytes serve as Shiga toxin carriers during the development of hemolytic uremic syndrome.Cellular & molecular biology letters · 2025Article
- A novel vaccine strategy using quick and easy conversion of bacterial pathogens to unnatural amino acid-auxotrophic suicide derivatives.Microbiology spectrum · 2024Article
- Red blood cell-derived arginase release in hemolytic uremic syndrome.Journal of translational medicine · 2024Article
- The ameliorative efficacy of Thymus vulgaris essential oil against Escherichia coli O157:H7-induced hematological alterations, hepatorenal dysfunction and immune-inflammatory disturbances in experimentally infected rats.Environmental science and pollution research international · 2022Article
- Effects of Niacin on Resistance to EnterotoxigenicFrontiers in nutrition · 2022Article
- IgG BindsFrontiers in immunology · 2022Article
- Annexin Induces Cellular Uptake of Extracellular Vesicles and Delays Disease inMicroorganisms · 2021Article
- A One Health Perspective for Defining and DecipheringComparative medicine · 2021Review
- Toll-Like Receptors in Acute Kidney Injury.International journal of molecular sciences · 2021Review
- Shiga toxin signals via ATP and its effect is blocked by purinergic receptor antagonism.Scientific reports · 2019Article
- Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS).Pediatric nephrology (Berlin, Germany) · 2018Review
- Bacterial Chat: Intestinal Metabolites and Signals in Host-Microbiota-Pathogen Interactions.Infection and immunity · 2017Review
- Review
- Pathogenesis of Colitis in Germ-Free Mice Infected With EHEC O157:H7.Veterinary pathology · 2017Article
- An Inhaled Inhibitor of Myristoylated Alanine-Rich C Kinase Substrate Reverses LPS-Induced Acute Lung Injury in Mice.American journal of respiratory cell and molecular biology · 2016Article
- The role of the antimicrobial peptide cathelicidin in renal diseases.Pediatric nephrology (Berlin, Germany) · 2015Review
- Article
- A novel mechanism of bacterial toxin transfer within host blood cell-derived microvesicles.PLoS pathogens · 2015Article
- Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptors (TLRs) are key factors of innate immunity that detect pathogen invasion and trigger a host response. TLR4 can mediate a response through adaptor molecules, MyD88 or TRIF. In the present study, streptomycin-treated MyD88(-/-), Tlr4(-/-), Trif (Lps2/Lps2), and C57BL/6 wild-type (WT) mice were infected with either Shiga toxin (Stx)-producing or non-producing Escherichia coli O157:H7. Moderate to severe clinical signs of disease developed in MyD88(-/-) (n = 21/21), Tlr4(-/-) (n = 12/16), Trif (Lps2/Lps2) (n = 7/15) and WT mice (n = 6/20) infected with Stx-producing E. coli O157:H7 but not in mice inoculated with the Stx non-producing strain (n = 0/54, P < 0.001). MyD88(-/-) mice infected with Stx-producing E. coli O157:H7 developed the most severe disease and had the highest bacterial burden. Hematological analysis of sick MyD88(-/-) mice showed reduced red blood cell counts and reticulocytosis, suggesting hemolysis. Thrombocytopenia developed in MyD88(-/-), Trif (Lps2/Lps2), and WT mice, and creatinine levels were elevated in both MyD88(-/-) and WT mice infected with the Stx-producing strain. Renal histopathology showed evidence of glomerular capillary congestion, tubular desquamation, and fibrinogen deposition, and intestinal histopathology showed mucosal injury, edema, and inflammation in sick mice. Administration of purified Stx2 to MyD88(-/-) and WT mice led to severe disease in both groups, suggesting that MyD88(-/-) mice are not more sensitive to Stx than WT mice. As MyD88(-/-) mice developed the most severe disease hematological and pathological changes, the results suggest that dysfunctional innate immune responses via MyD88 enhanced Stx-induced disease.
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