ArticleInfection and immunity2014
Protection from Clostridium difficile infection in CD4 T Cell- and polymeric immunoglobulin receptor-deficient mice.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 38 citations in OpenAlex.
- Trial
- Article
- The interplay between host immunity andmBio · 2025Review
- Fiber- and acetate-mediated modulation of MHC-II expression on intestinal epithelium protects from Clostridioides difficile infection.Cell host & microbe · 2025Article
- A Mouse Model of MildMicroorganisms · 2024Article
- Reviewing theMicroorganisms · 2024Review
- Host Immunity and Immunization Strategies for Clostridioides difficile Infection.Clinical microbiology reviews · 2023Review
- Review
- Heterologous Immunity Between SARS-CoV-2 and Pathogenic Bacteria.Frontiers in immunology · 2022Article
- Assessment of independent comorbidities and comorbidity measures in predicting healthcare facility-onset Clostridioides difficile infection in Kenya.PLOS global public health · 2022Article
- Translational Aspects of the Immunology of Clostridioides difficile Infection: Implications for Pediatric Populations.Journal of the Pediatric Infectious Diseases Society · 2021Review
- Host immunity modulates the efficacy of microbiota transplantation for treatment of Clostridioides difficile infection.Nature communications · 2021Article
- Outbreaks of Typhlocolitis Caused by Hypervirulent Group ST1Comparative medicine · 2020Article
- Bacteria That Cause Enteric Diseases Stimulate Distinct Humoral Immune Responses.Frontiers in immunology · 2020Review
- Type 3 Immunity during Clostridioides difficile Infection: Too Much of a Good Thing?Infection and immunity · 2019Review
- Proteomic Analysis on Exosomes Derived from Patients' Sera Infected with Echinococcus granulosus.The Korean journal of parasitology · 2019Article
- IL-33 drives group 2 innate lymphoid cell-mediated protection during Clostridium difficile infection.Nature communications · 2019Article
- The Gut Microbiota Is Associated with Clearance of Clostridium difficile Infection Independent of Adaptive Immunity.mSphere · 2019Article
- Article
- Natural Secretory Immunoglobulins Promote Enteric Viral Infections.Journal of virology · 2018Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Clostridium difficile rivals methicillin-resistant Staphylococcus aureus as the primary hospital-acquired infection. C. difficile infection (CDI) caused by toxins A and/or B can manifest as mild diarrhea to life-threatening pseudomembranous colitis. Although most patients recover fully from CDI, ~20% undergo recurrent disease. Several studies have demonstrated a correlation between anti-toxin antibody (Ab) and decreased recurrence; however, the contributions of the systemic and mucosal Ab responses remain unclear. Our goal was to use the CDI mouse model to characterize the protective immune response to C. difficile. C57BL/6 mice infected with epidemic C. difficile strain BI17 developed protective immunity against CDI and did not develop CDI upon rechallenge; they generated systemic IgG and IgA as well as mucosal IgA Ab to toxin. To determine if protective immunity to C. difficile could be generated in immunodeficient individuals, we infected CD4(-/-) mice and found that they generated both mucosal and serum IgA anti-toxin Abs and were protected from CDI upon rechallenge, with protection dependent on major histocompatibility complex class II (MHCII) expression; no IgG anti-toxin Ab was found. We found that protection was likely due to neutralizing mucosal IgA Ab. In contrast, pIgR(-/-) mice, which lack the receptor to transcytose polymeric Ab across the epithelium, were also protected from CDI, suggesting that although mucosal anti-toxin Ab may contribute to protection, it is not required. We conclude that protection from CDI can occur by several mechanisms and that the mechanism of protection is determined by the state of immunocompetence of the host.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.