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      KGF pretreatment decreases B7 and granzyme B expression and hastens repair in lungs of mice after allogeneic BMT.

      American Journal of Physiology - Lung Cellular and Molecular Physiology

      Transplantation Conditioning, Antigens, CD, genetics, Antigens, CD80, Antigens, CD86, Bone Marrow Transplantation, adverse effects, immunology, Fibroblast Growth Factor 10, Fibroblast Growth Factor 7, Fibroblast Growth Factors, Gene Expression, Granzymes, Growth Substances, pharmacology, Hypersensitivity, In Situ Hybridization, Interleukin-13, blood, Interleukin-4, Animals, Interleukin-6, Macrophages, Alveolar, Membrane Glycoproteins, Mice, Mice, Inbred C57BL, Microscopy, Electron, Monocytes, Pneumonia, etiology, Pulmonary Alveoli, enzymology, ultrastructure, RNA, Messenger, analysis, Serine Endopeptidases, Th2 Cells

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          Abstract

          We investigated keratinocyte growth factor (KGF) as a pretreatment therapy for idiopathic pneumonia syndrome (IPS) generated as a result of lung damage and allogeneic T cell-dependent inflammatory events occurring in the early peri-bone marrow (BM) transplant (BMT) period. B10.BR (H2(k)) recipient mice were transplanted with C57BL/6 (H2(b)) BM with spleen cells after lethal irradiation with and without cyclophosphamide conditioning with and without subcutaneous KGF pretreatment. KGF-pretreated mice had fewer injured alveolar type II (ATII) cells at the time of BMT and exhibited ATII cell hyperplasia at day 3 post-BMT. The composition of infiltrating cells on day 7 post-BMT was not altered by KGF pretreatment, but the frequencies of cells expressing the T-cell costimulatory molecules B7.1 and B7.2 and mRNA for the cytolysin granzyme B (usually increased in IPS) were decreased by KGF. Sera from KGF-treated mice had increases in the Th2 cytokines interleukin (IL)-4, IL-6, and IL-13 4 days after cessation of KGF administration (i.e., at the time of BMT). These data suggest that KGF hinders IPS by two modes: 1) stimulation of alveolar epithelialization and 2) attenuation of immune-mediated injury as a consequence of failure to upregulate cytolytic molecules and B7 ligand expression and the induction of anti-inflammatory Th2 cytokines in situ.

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