ArticleInfection and immunity2013
Loss of mitochondrial protein Fus1 augments host resistance to Acinetobacter baumannii infection.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 19 citations in OpenAlex.
- Loss of Mitochondrial Tusc2/Fus1 Triggers a Brain Pro-Inflammatory Microenvironment and Early Spatial Memory Impairment.International journal of molecular sciences · 2024Article
- Mitochondrial Fus1/Tusc2 and cellular Ca2Cancer gene therapy · 2022Review
- Lipocalin-2 is an essential component of the innate immune response to Acinetobacter baumannii infection.PLoS pathogens · 2022Article
- Biological sex influences susceptibility to Acinetobacter baumannii pneumonia in mice.JCI insight · 2020Article
- Host Innate Immune Responses toFrontiers in cellular and infection microbiology · 2020Review
- Transcriptome Profiling of Lung Innate Immune Responses Potentially Associated With the Pathogenesis ofFrontiers in immunology · 2020Article
- Novel Role of the Mitochondrial Protein Fus1 in Protection from Premature Hearing Loss via Regulation of Oxidative Stress and Nutrient and Energy Sensing Pathways in the Inner Ear.Antioxidants & redox signaling · 2017Article
- Tumor suppressor candidate 2 (TUSC2, FUS-1) and human cancers.Discovery medicine · 2017Review
- Article
- RAGE-Mediated Suppression of Interleukin-10 Results in Enhanced Mortality in a Murine Model of Acinetobacter baumannii Sepsis.Infection and immunity · 2017Article
- Future Directions and Molecular Basis of Ventilator Associated Pneumonia.Canadian respiratory journal · 2017Review
- Clinical and Pathophysiological Overview of Acinetobacter Infections: a Century of Challenges.Clinical microbiology reviews · 2017Review
- Acinetobacter baumannii Infection and IL-17 Mediated Immunity.Mediators of inflammation · 2016Review
- Fus1 KO Mouse As a Model of Oxidative Stress-Mediated Sporadic Alzheimer's Disease: Circadian Disruption and Long-Term Spatial and Olfactory Memory Impairments.Frontiers in aging neuroscience · 2016Article
- Toll-Like Receptor 9 Contributes to Defense against Acinetobacter baumannii Infection.Infection and immunity · 2015Article
- Mitochondria, calcium, and tumor suppressor Fus1: At the crossroad of cancer, inflammation, and autoimmunity.Oncotarget · 2015Review
- Cellular oxidative stress response mediates radiosensitivity in Fus1-deficient mice.Cell death & disease · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Fus1 is a tumor suppressor protein with recently described immunoregulatory functions. Although its role in sterile inflammation is being elucidated, its role in regulating immune responses to infectious agents has not been examined. We used here a murine model of Acinetobacter baumannii pneumonia to identify the role of Fus1 in antibacterial host defenses. We found that the loss of Fus1 in mice results in significantly increased resistance to A. baumannii pneumonia. We observed earlier and more robust recruitment of neutrophils and macrophages to the lungs of infected Fus1(-/-) mice, with a concomitant increase in phagocytosis of invading bacteria and more rapid clearance. Such a prompt and enhanced immune response to bacterial infection in Fus1(-/-) mice stems from early activation of proinflammatory pathways (NF-κB and phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin [mTOR]), most likely due to significantly increased mitochondrial membrane potential and mitochondrial reactive oxygen species production. Significant early upregulation of interleukin-17 (IL-17) in Fus1(-/-) immune cells was also observed, together with significant downregulation of IL-10. Depletion of neutrophils eliminates the enhanced antibacterial defenses of the Fus1(-/-) mice, suggesting that ultimately it is the enhanced immune cell recruitment that mediates the increased resistance of Fus1(-/-) mice to A. baumannii pneumonia. Taken together, our data define the novel role for Fus1 in the immune response to A. baumannii pneumonia and highlight new avenues for immune modulating therapeutic targets for this treatment-resistant nosocomial pathogen.
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.