ArticleJournal of immunology (Baltimore, Md. : 1950)2016
Alveolar Epithelial Cell-Derived Prostaglandin E2 Serves as a Request Signal for Macrophage Secretion of Suppressor of Cytokine Signaling 3 during Innate Inflammation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. 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
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
29 citing papers in PubMed, 40 citations in OpenAlex.
- Oxylipin Profiling of Airway Structural Cells Is Unique and Modified by Relevant Stimuli.Journal of proteome research · 2025Article
- Alveolar Macrophages in Viral Respiratory Infections: Sentinels and Saboteurs of Lung Defense.International journal of molecular sciences · 2025Review
- Circular RNA DHTKD1 targets miR‑338‑3p/ETS1 axis to regulate the inflammatory response in human bronchial epithelial cells.Experimental and therapeutic medicine · 2023Article
- Phagocytosis is a primary determinant of pulmonary clearance of clinicalFrontiers in cellular and infection microbiology · 2023Article
- Age-induced prostaglandin ENature communications · 2022Article
- ATP citrate lyase links increases in glycolysis to diminished release of vesicular suppressor of cytokine signaling 3 by alveolar macrophages.Biochimica et biophysica acta. Molecular basis of disease · 2022Article
- Circulating cardiomyocyte-derived extracellular vesicles reflect cardiac injury during systemic inflammatory response syndrome in mice.Cellular and molecular life sciences : CMLS · 2022Article
- The Fusion Protein rFlaA:Betv1 Modulates DC Responses by a p38-MAPK and COX2-Dependent Secretion of PGECells · 2021Article
- Myeloid-Specific Deficiency ofJournal of immunology (Baltimore, Md. : 1950) · 2021Article
- Alveolar macrophage-derived extracellular vesicles inhibit endosomal fusion of influenza virus.The EMBO journal · 2020Article
- Electric Stimulation Hyperthermia Relieves InflammationThe world journal of men's health · 2020Article
- Oxidative Inactivation of the Proteasome Augments Alveolar Macrophage Secretion of Vesicular SOCS3.Cells · 2020Article
- Resident alveolar macrophage-derived vesicular SOCS3 dampens allergic airway inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Transcriptional regulation of the IL-13Rα2 gene in human lung fibroblasts.Scientific reports · 2020Article
- Alveolar macrophage secretion of vesicular SOCS3 represents a platform for lung cancer therapeutics.JCI insight · 2019Article
- Article
- Exhalative Breath Markers Do Not Offer for Diagnosis of Interstitial Lung Diseases: Data from the European IPF Registry (eurIPFreg) and Biobank.Journal of clinical medicine · 2019Article
- TBC1D3 regulates the payload and biological activity of extracellular vesicles that mediate tissue repair.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Alveolar Macrophages in the Resolution of Inflammation, Tissue Repair, and Tolerance to Infection.Frontiers in immunology · 2018Review
- Eicosanoid Control Over Antigen Presenting Cells in Asthma.Frontiers in immunology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Preservation of gas exchange mandates that the pulmonary alveolar surface restrain unnecessarily harmful inflammatory responses to the many challenges to which it is exposed. These responses reflect the cross-talk between alveolar epithelial cells (AECs) and resident alveolar macrophages (AMs). We recently determined that AMs can secrete suppressor of cytokine signaling (SOCS) proteins within microparticles. Uptake of these SOCS-containing vesicles by epithelial cells inhibits cytokine-induced STAT activation. However, the ability of epithelial cells to direct AM release of SOCS-containing vesicles in response to inflammatory insults has not been studied. In this study, we report that SOCS3 protein was elevated in bronchoalveolar lavage fluid of both virus- and bacteria-infected mice, as well as in an in vivo LPS model of acute inflammation. In vitro studies revealed that AEC-conditioned medium (AEC-CM) enhanced AM SOCS3 secretion above basal levels. Increased amounts of PGE2 were present in AEC-CM after LPS challenge, and both pharmacologic inhibition of PGE2 synthesis in AECs and neutralization of PGE2 in AEC-CM implicated this prostanoid as the major AEC-derived factor mediating enhanced AM SOCS3 secretion. Moreover, pharmacologic blockade of PGE2 synthesis or genetic deletion of a PGE2 synthase similarly attenuated the increase in bronchoalveolar lavage fluid SOCS3 noted in lungs of mice challenged with LPS in vivo. These results demonstrate a novel tunable form of cross-talk in which AECs use PGE2 as a signal to request SOCS3 from AMs to dampen their endogenous inflammatory responses during infection.
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.