ArticleBiology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation2017
Targeting the Canonical Nuclear Factor-κB Pathway with a High-Potency IKK2 Inhibitor Improves Outcomes in a Mouse Model of Idiopathic Pneumonia Syndrome.
Article in Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Therapeutic impact of mesenchymal stem cells on idiopathic pneumonia syndrome after allogeneic hematopoietic stem cell transplantation.International journal of hematology · 2025Article
- Prevention of non-infectious pulmonary complications after intra-bone marrow stem cell transplantation in mice.PloS one · 2022Article
- Impaired bone marrow B-cell development in mice with a bronchiolitis obliterans model of cGVHD.Blood advances · 2018Article
- ETS1 is associated with cisplatin resistance through IKKα/NF-κB pathway in cell line MDA-MB-231.Cancer cell international · 2018Article
- Ginsenoside Rb1 Alleviates Lipopolysaccharide-Induced Inflammatory Injury by Downregulating miR-222 in WI-38 Cells.Cell transplantationArticle
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Idiopathic pneumonia syndrome (IPS) is a noninfectious inflammatory disorder of the lungs that occurs most often after fully myeloablative allogeneic hematopoietic stem cell transplantation (HSCT). IPS can be severe and is associated with high 1-year mortality rates despite existing therapies. The canonical nuclear factor-(NF) κB signaling pathway has previously been linked to several inflammatory disorders of the lung, including asthma and lung allograft rejection. It has never been specifically targeted as a novel IPS treatment approach, however. Here, we report that the IκB kinase 2 (IKK2) antagonist BAY 65-5811 or "compound A," a highly potent and specific inhibitor of the NF-κB pathway, was able to improve median survival times and recipient oxygenation in a well-described mouse model of IPS. Compound A impaired the production of the proinflammatory chemokines CCL2 and CCL5 within the host lung after transplantation. This resulted in significantly lower numbers of donor lung infiltrating CD4
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