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      Acute lung injury after allogeneic stem cell transplantation: is the lung a target of acute graft-versus-host disease?

      Bone Marrow Transplantation

      Transplantation, Homologous, mortality, adverse effects, Stem Cell Transplantation, etiology, Pneumonia, Lung Injury, pathology, Lung, Humans, Graft vs Host Disease, therapeutic use, Anti-Bacterial Agents

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          Abstract

          Allogeneic hematopoietic stem cell transplantation (SCT) is an important therapeutic option for a number of malignant and nonmalignant conditions but the broader application of this treatment strategy is limited by several side effects. In particular, diffuse lung injury is a major complication of SCT that responds poorly to standard therapeutic approaches and significantly contributes to transplant-related morbidity and mortality. Historically, approximately 50% of all pneumonias seen after SCT have been secondary to infection, but the judicious use of broad-spectrum antimicrobial prophylaxis in recent years has tipped the balance of pulmonary complications from infectious to noninfectious causes. This mini review will discuss the definition, risk factors and pathogeneses of noninfectious lung injury that occurs early after allogeneic SCT.

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          Chemokines--chemotactic cytokines that mediate inflammation.

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            Defective LPS Signaling in C3H/HeJ and C57BL/10ScCr Mice: Mutations in Tlr4 Gene

             A Poltorak (1998)
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              Endothelial apoptosis as the primary lesion initiating intestinal radiation damage in mice.

              Gastrointestinal (GI) tract damage by chemotherapy or radiation limits their efficacy in cancer treatment. Radiation has been postulated to target epithelial stem cells within the crypts of Lieberkühn to initiate the lethal GI syndrome. Here, we show in mouse models that microvascular endothelial apoptosis is the primary lesion leading to stem cell dysfunction. Radiation-induced crypt damage, organ failure, and death from the GI syndrome were prevented when endothelial apoptosis was inhibited pharmacologically by intravenous basic fibroblast growth factor (bFGF) or genetically by deletion of the acid sphingomyelinase gene. Endothelial, but not crypt, cells express FGF receptor transcripts, suggesting that the endothelial lesion occurs before crypt stem cell damage in the evolution of the GI syndrome. This study provides a basis for new approaches to prevent radiation damage to the bowel.
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                Author and article information

                Journal
                10.1038/sj.bmt.1704629
                15300233

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