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Mouse strains deficient in adaptive and innate immune functions, such as NSG, NSG-SGM3, and NBSGW, are highly susceptible to opportunistic infections. Over a period of 7 mo, 1,193 mice from the above 3 strains in an SPF barrier were observed with mild loose stool (LS). Affected mice had minimal weight loss and mortality. Histopathology revealed erosion of the jejunal villi with neutrophilic inflammation and Gram-positive bacterial rods adhering to the cecal mucosa with varying degrees of mucosal hyperplasia, epithelial vacuolation, and apoptosis. Anaerobic culture revealed a clostridial species that could not be speciated using standard biochemical phenotyping. Further, Clostridioides difficle and Clostridioides perfringens ELISA on intestinal contents were negative for toxins. We performed a challenge study by exposing naïve NSG mice to dirty bedding from affected cages; metagenomics on pre- and postchallenge feces identified and associated the etiopathogenesis to Clostridioides cuniculi. Whole genome sequencing and phylogenetic analysis confirmed the identity of C. cuniculi. The isolate was sensitive to trimethoprim-sulfamethoxazole (TMS). TMS was effective in abrogating signs of LS and clearing infection in mice in studies. A probe-based real-time PCR specific for C. cuniculi was established. This assay was used to screen environmental and fomite contamination and potential use in rack-level screening. We traced the source of the outbreak to a NBSGW breeding colony. However, in our observation, spontaneous C. cuniculi-induced disease was only seen in the presence of an irradiated diet in the breeding NBSGW strain and not in the breeding colonies of NSG or NSG-SGM3 strains. Interestingly, we observed that exposure to infected feces from NBSGW-induced LS in both NSG and NSG-SGM3 mice. This investigation provides insights into the etiopathogenesis and probable source of sporadic clostridial infections in immunodeficient mice and lays the groundwork for its prevention and surveillance in immunodeficient mouse colonies.
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http://dx.doi.org/10.30802/AALAS-JAALAS-25-030 | DOI Listing |
Front Immunol
September 2025
Division of Allergy and Clinical Immunology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
NSG-SGM3 humanized mouse models are well-suited for studying human immune physiology but are technically challenging and expensive. We previously characterized a simplified NSG-SGM3 mouse, engrafted with human donor CD34 hematopoietic stem cells without receiving prior bone marrow ablation or human secondary lymphoid tissue implantation, that still retains human mast cell- and basophil-dependent passive anaphylaxis responses. Its capacities for human antibody production and human B cell maturation, however, remain unknown.
View Article and Find Full Text PDFTrends Immunol
August 2025
Cell Death Signaling Laboratory, Department of Biomedical Sciences, University of Antwerp, Antwerp, Belgium; VIB-UGent Center for Inflammation Research, VIB, 9052 Ghent, Belgium; Department of Internal Medicine and Paediatrics, Ghent University, 9052 Ghent, Belgium. Electronic address: andy.wullaert
Humanized mouse models with transgenic expression of human myelopoiesis-supporting growth factors have enhanced human myeloid cell engraftment and improved the study of human innate immune responses. Here, we discuss the remaining challenges associated with studying innate immunity in humanized NSG-SGM3 and MISTRG mice, as well as potential advances to overcome them.
View Article and Find Full Text PDFJ Am Assoc Lab Anim Sci
May 2025
1Animal Resource Center, St. Jude Children's Research Hospital, Memphis, Tennessee.
Mouse strains deficient in adaptive and innate immune functions, such as NSG, NSG-SGM3, and NBSGW, are highly susceptible to opportunistic infections. Over a period of 7 mo, 1,193 mice from the above 3 strains in an SPF barrier were observed with mild loose stool (LS). Affected mice had minimal weight loss and mortality.
View Article and Find Full Text PDFJ Allergy Clin Immunol
July 2025
Division of Allergy and Clinical Immunology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Md. Electronic address:
Background: There is a need for novel rescue therapies that can reduce morbidity and/or mortality from acute anaphylaxis. Given prior data showing that oral inhibitors of Bruton tyrosine kinase (BTK) can act rapidly as preventive agents for food-induced anaphylaxis in mice and humans, we hypothesized that these compounds could also abort ongoing acute IgE-mediated anaphylactic reactions.
Methods: Primary human mast cells and basophils were stimulated with anti-IgE, treated with the BTK inhibitor acalabrutinib, and assessed for activation and degranulation.
Cell Death Dis
July 2025
Department of Personalized Medicine and Rare Diseases, Medfuture Institute for Biomedical Research, Iuliu Hațieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Myelodysplastic syndromes (MDS) are heterogeneous hematopoietic stem cell disorders defined by ineffective hematopoiesis, multilineage dysplasia, and risk of progression to acute myeloid leukemia. Improvements have been made to identify recurrent genetic mutations and their functional roles, but translating this into preclinical models is still difficult. Traditional murine systems lack the human-specific cytokine support and microenvironmental support that is necessary to reproduce MDS pathophysiology.
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