ArticleInfection and immunity2004
Exogenous gamma and alpha/beta interferon rescues human macrophages from cell death induced by Bacillus anthracis.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- Role of NLRs in the Regulation of Type I Interferon Signaling, Host Defense and Tolerance to Inflammation.International journal of molecular sciences · 2021Review
- Interferons: Tug of War Between Bacteria and Their Host.Frontiers in cellular and infection microbiology · 2021Review
- The Protective Role of Type I Interferons in the Gastrointestinal Tract.Frontiers in immunology · 2017Review
- Citrobacter rodentium NleB Protein Inhibits Tumor Necrosis Factor (TNF) Receptor-associated Factor 3 (TRAF3) Ubiquitination to Reduce Host Type I Interferon Production.The Journal of biological chemistry · 2016Article
- Type I interferons in infectious disease.Nature reviews. Immunology · 2015Review
- Type I IFN exhaustion is a host defence protecting against secondary bacterial infections.Scandinavian journal of immunology · 2013Review
- Review
- Mechanisms of NK cell-macrophage Bacillus anthracis crosstalk: a balance between stimulation by spores and differential disruption by toxins.PLoS pathogens · 2012Article
- Type I interferon signaling regulates the composition of inflammatory infiltrates upon infection with Listeria monocytogenes.Cellular immunology · 2012Article
- DNase Sda1 allows invasive M1T1 Group A Streptococcus to prevent TLR9-dependent recognition.PLoS pathogens · 2012Article
- Comparison of WTC dust size on macrophage inflammatory cytokine release in vivo and in vitro.PloS one · 2012Article
- The role of innate immune signals in immunity to Brucella abortus.Frontiers in cellular and infection microbiology · 2012Review
- MyD88 and STING signaling pathways are required for IRF3-mediated IFN-β induction in response to Brucella abortus infection.PloS one · 2011Article
- Neutrophils activate alveolar macrophages by producing caspase-6-mediated cleavage of IL-1 receptor-associated kinase-M.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Interferon-inducible CXC chemokines directly contribute to host defense against inhalational anthrax in a murine model of infection.PLoS pathogens · 2010Article
- Type I interferon: friend or foe?The Journal of experimental medicine · 2010Review
- Conidia but not yeast cells of the fungal pathogen Histoplasma capsulatum trigger a type I interferon innate immune response in murine macrophages.Infection and immunity · 2010Article
- Resistance of human alveolar macrophages to Bacillus anthracis lethal toxin.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- NOD2, RIP2 and IRF5 play a critical role in the type I interferon response to Mycobacterium tuberculosis.PLoS pathogens · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
During the recent bioterrorism-related outbreaks, inhalational anthrax had a 45% mortality in spite of appropriate antimicrobial therapy, underscoring the need for better adjuvant therapies. The variable latency between exposure and development of disease suggests an important role for the host's innate immune response. Alveolar macrophages are likely the first immune cells exposed to inhalational anthrax, and the interferon (IFN) response of these cells comprises an important arm of the host innate immune response to intracellular infection with Bacillus anthracis. Furthermore, IFNs have been used as immunoadjuvants for treatment of another intracellular pathogen, Mycobacterium tuberculosis. We established a model of B. anthracis infection with the Sterne strain (34F(2)) which contains lethal toxin (LeTx). 34F(2) was lethal to murine and human macrophages. Treatment with IFNs significantly improved cell viability and reduced the number of germinated intracellular spores. Infection with 34F(2) failed to induce the latent transcription factors signal transducer and activators of transcription 1 (STAT1) and ISGF-3, which are central to the IFN response. Furthermore, 34F(2) reduced STAT1 activation in response to exogenous alpha/beta IFN, suggesting direct inhibition of IFN signaling. Even though 34F(2) has LeTx, there was no mitogen-activated protein kinase kinase 3 cleavage and p38 was normally induced, suggesting that these early effects of B. anthracis infection in macrophages are independent of LeTx. These data suggest an important role for both IFNs in the control of B. anthracis and the potential benefit of using exogenous IFN as an immunoadjuvant therapy.
Indexed as
Identifiers
What OpenQuestion holds
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.