In one paragraphArticle in Science signaling, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 53% of its field
1 · What the graph read from itWhat 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.
2 · The registryThe 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.
3 · Its place in the literatureWho cites it
0 citing papers in PubMed, 2 citations in OpenAlex.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
20 authors at 5 institutions in 1 country.
Tamara T HaqueDepartment of Microbiology and Immunology, Virginia Commonwealth University, Richmond, VA 23298, USA.ORCID 0000-0003-4436-9558 Marcela T TaruselliDepartment of Microbiology and Immunology, Virginia Commonwealth University, Richmond, VA 23298, USA.ORCID 0000-0002-7965-4335 Jordan M DaileyDepartment of Microbiology and Immunology, Virginia Commonwealth University, Richmond, VA 23298, USA.
Paula A Gajewski-KurdzielDepartment of Biomedical Science, Charles E. Schmidt College of Medicine, Florida Atlantic University, Jupiter, FL 33458, USA.
Matthew P ZellnerDepartment of Microbiology and Immunology, Virginia Commonwealth University, Richmond, VA 23298, USA.
Daniel J StephensonDepartment of Cell Biology, University of Virginia-School of Medicine, Charlottesville, VA 22903, USA.ORCID 0000-0002-5698-3400 H Patrick MacKnightDepartment of Cell Biology, University of Virginia-School of Medicine, Charlottesville, VA 22903, USA.
David B StrausDepartment of Biology, Virginia Commonwealth University, Richmond, VA 23284, USA.
Kaitlyn G JacksonDepartment of Microbiology and Immunology, Virginia Commonwealth University, Richmond, VA 23298, USA.ORCID 0000-0003-2663-9593 Alena P ChumanevichDepartment of Pathology, Microbiology and Immunology, University of South Carolina School of Medicine, Columbia, SC 29208, USA.ORCID 0000-0002-9654-1949 Yoshihiro FukuokaDepartment of Internal Medicine, Virginia Commonwealth University, Richmond, VA 23298, USA.
Lawrence B SchwartzDepartment of Internal Medicine, Virginia Commonwealth University, Richmond, VA 23298, USA.
Randy D BlakelyDepartment of Biomedical Science, Charles E. Schmidt College of Medicine, Florida Atlantic University, Jupiter, FL 33458, USA.
Carole A OskeritzianDepartment of Pathology, Microbiology and Immunology, University of South Carolina School of Medicine, Columbia, SC 29208, USA.ORCID 0000-0003-1380-9186 Charles E ChalfantDepartment of Cell Biology, University of Virginia-School of Medicine, Charlottesville, VA 22903, USA.ORCID 0000-0002-5844-5235 Rebecca K MartinDepartment of Microbiology and Immunology, Virginia Commonwealth University, Richmond, VA 23298, USA.ORCID 0000-0001-9948-5463 Virginia Commonwealth University · USFlorida Atlantic University · USUniversity of South Carolina · USUniversity of Virginia · USUnited States Department of Veterans Affairs · US
Funding
The roles of ceramide and its derivatives in A. phagocytophilum pathogenesisR01AI139072 · NIAID · VIRGINIA COMMONWEALTH UNIVERSITY · PI CHARLES E. CHALFANT, Jason A Carlyon · 2018 to 2026
$5.7MThe functional role of the cPLA2alpha/C1P interaction in sepsis resolutionR01HL125353 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI BROWN, RHODERICK E, CHALFANT, CHARLES E. · 2014 to 2018
$4.0MGGT Targeting Suppresses Mast Cell Activation by IgE and IL-33R01AI138495 · NIAID · VIRGINIA COMMONWEALTH UNIVERSITY · PI RYAN, JOHN J · 2018 to 2022
$2.2MiPLA2beta-mediated alternative splicing and -cell death in type 1 diabetesR01DK126444 · NIDDK · UNIVERSITY OF VIRGINIA · PI CHALFANT, CHARLES E., EIZIRIK, DECIO LAKS · 2021 to 2024
$2.0MP2X3 is a Female-Dominant Amplifier of Mast Cell FunctionR01AI164710 · NIAID · VIRGINIA COMMONWEALTH UNIVERSITY · PI RYAN, JOHN J · 2021 to 2025
$1.8MMast Cell S1P Receptor2 in the initiation and progression of chronic inflammationR01AI095494 · NIAID · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI OSKERITZIAN, CAROLE A · 2012 to 2015
$1.4MMicroRNAs in atopic dermatitis pathogenesis: a role for mast cell and sphingosine-1-phosphate?R21AR067996 · NIAMS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI OSKERITZIAN, CAROLE A · 2016 to 2017
$323kRole of serotonergic IL-1R1 in modulating physiological and behavioral responses to peripheral inflammationF32MH120966 · NIMH · FLORIDA ATLANTIC UNIVERSITY · PI KURDZIEL, PAULA ANN · 2020 to 2022
$203kSSRI's Suppress IgE-Mediated Mast Cell FunctionF31AI140609 · NIAID · VIRGINIA COMMONWEALTH UNIVERSITY · PI HAQUE, TAMARA TASMIA · 2019 to 2019
$28kBLRD Research Career Scientist Award ApplicationIK6BX004603 · VA · VA VETERANS ADMINISTRATION HOSPITAL · PI CHALFANT, CHARLES E. · 2019 to 2025
–The role of RNA splicing in non-small cell lung cancerI01BX001792 · VA · VA VETERANS ADMINISTRATION HOSPITAL · PI CHALFANT, CHARLES E. · 2013 to 2024
–BLRD VA I01 BX001792BLRD VA IK6 BX004603NHLBI NIH HHS R01 HL125353NIAID NIH HHS F31 AI140609NIAID NIH HHS R01 AI095494NIAID NIH HHS R01 AI138495NIAID NIH HHS R01 AI139072NIAID NIH HHS R01 AI164710NIAMS NIH HHS R21 AR067996NIDDK NIH HHS R01 DK126444NIMH NIH HHS F32 MH120966
6 · The paper itselfAbstract
There is a clinical need for new treatment options addressing allergic disease. Selective serotonin reuptake inhibitors (SSRIs) are a class of antidepressants that have anti-inflammatory properties. We tested the effects of the SSRI fluoxetine on IgE-induced function of mast cells, which are critical effectors of allergic inflammation. We showed that fluoxetine treatment of murine or human mast cells reduced IgE-mediated degranulation, cytokine production, and inflammatory lipid secretion, as well as signaling mediated by the mast cell activator ATP. In a mouse model of systemic anaphylaxis, fluoxetine reduced hypothermia and cytokine production. Fluoxetine was also effective in a model of allergic airway inflammation, where it reduced bronchial responsiveness and inflammation. These data show that fluoxetine suppresses mast cell activation by impeding an FcɛRI-ATP positive feedback loop and support the potential repurposing of this SSRI for use in allergic disease.
Indexed as
FluoxetineMast CellsAdenosine TriphosphateAnimalsCytokinesFeedbackHumansImmunoglobulin EInflammationMiceAdenosine TriphosphateCytokinesFluoxetineImmunoglobulin E
Identifiers
PMID37699080
PMCPMC10759315
OpenAlexW4386634082
What OpenQuestion holds
Textmetadata
LicenceTDM
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