ArticleJournal of immunology (Baltimore, Md. : 1950)2010
A role for IL-1 receptor-associated kinase-M in prostaglandin E2-induced immunosuppression post-bone marrow transplantation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Pooled it
- Activation of the endoplasmic reticulum stress regulator IRE1α compromises pulmonary host defenses.Cell reports · 2025Article
- The IRAK-M death domain: a tale of three surfaces.Frontiers in molecular biosciences · 2023Article
- The Fusion Protein rFlaA:Betv1 Modulates DC Responses by a p38-MAPK and COX2-Dependent Secretion of PGECells · 2021Article
- Effects of Hematopoietic Cell Transplantation on the Pulmonary Immune Response to Infection.Frontiers in pediatrics · 2021Review
- Cytokine Cocktail Promotes Alveolar Macrophage Reconstitution and Functional Maturation in a Murine Model of Haploidentical Bone Marrow Transplantation.Frontiers in immunology · 2021Article
- Experimental Models of Infectious Pulmonary Complications Following Hematopoietic Cell Transplantation.Frontiers in immunology · 2021Review
- Cancer; an induced disease of twentieth century! Induction of tolerance, increased entropy and 'Dark Energy': loss of biorhythms (Anabolism v. Catabolism).Clinical and translational medicine · 2018Article
- Prostaglandin EPharmacology & therapeutics · 2018Review
- Elevated prostaglandin EMucosal immunology · 2018Article
- Interleukin-36γ and IL-36 receptor signaling mediate impaired host immunity and lung injury in cytotoxic Pseudomonas aeruginosa pulmonary infection: Role of prostaglandin E2.PLoS pathogens · 2017Article
- Article
- Prostaglandin EFrontiers in physiology · 2017Review
- Targeting Inhibitor of Apoptosis Proteins Protects from Bleomycin-Induced Lung Fibrosis.American journal of respiratory cell and molecular biology · 2016Article
- Prostaglandin E2 Production and T Cell Function in Mouse Adenovirus Type 1 Infection following Allogeneic Bone Marrow Transplantation.PloS one · 2015Article
- Transforming growth factor-β induces microRNA-29b to promote murine alveolar macrophage dysfunction after bone marrow transplantation.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- The structure function of the death domain of human IRAK-M.Cell communication and signaling : CCS · 2014Article
- Prostaglandin E2 reduces Toll-like receptor 4 expression in alveolar macrophages by inhibition of translation.American journal of respiratory cell and molecular biology · 2014Article
- γ-Herpes virus-68, but not Pseudomonas aeruginosa or influenza A (H1N1), exacerbates established murine lung fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Following immune reconstitution, hematopoietic stem cell transplant patients often display reduced immune function and are especially susceptible to lung infections. In a mouse model of syngeneic bone marrow transplantation (BMT), we previously reported that PGE(2) is overproduced in lungs of BMT mice, significantly impairing host defense against Pseudomonas aeruginosa. This impairment in host defense post-BMT is also marked by diminished alveolar macrophage (AM) phagocytosis, bacterial killing, and production of TNF-alpha and cysteinyl leukotrienes. However, a mechanism by which overproduction of PGE(2) suppresses pulmonary host defense post-BMT is unknown. As IL-1R-associated kinase (IRAK)-M is a known inhibitor of MyD88-dependent IL-1R/TLR signaling and macrophage function, we sought to determine whether IRAK-M is involved in PGE(2)-induced immunosuppression post-BMT. We found that IRAK-M expression is elevated 3.5-fold in BMT AMs relative to control AMs, and this is related to AM overproduction of PGE(2). Furthermore, genetic ablation of IRAK-M in the bone marrow of BMT mice restores host defense against P. aeruginosa. Despite AM overproduction of PGE(2) and elevated E prostanoid 2 receptor expression, AM phagocytosis, killing, and production of cysteinyl leukotrienes and TNF-alpha are restored in the absence of IRAK-M post-BMT. Also, treatment with PGE(2) does not inhibit AM phagocytosis in the absence of IRAK-M. These data suggest that the absence of IRAK-M in the hematopoietic compartment post-BMT enhances pulmonary host defense and mitigates AM sensitivity to the inhibitory effects of PGE(2). Therefore, strategies to limit IRAK-M elevation post-BMT may be efficacious in reducing patient susceptibility to infection.
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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.