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Prepublished online as a Blood First Edition Paper on January 2, 2003; DOI 10.1182/blood-2002-08-2465. This Article Full Text (PDF) All Versions of this Article: 2002-08-2465v1 101/9/3714    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Panoskaltsis-Mortari, A. Articles by Blazar, B. R Search for Related Content PubMed PubMed Citation Articles by Panoskaltsis-Mortari, A. Articles by Blazar, B. R Social Bookmarking                   What's this? Submitted August 14, 2002 Accepted November 22, 2002 Acceleration of idiopathic pneumonia syndrome (IPS) in the absence of donor MIP-1 (CCL3) post-allogeneic BMT in mice Angela Panoskaltsis-Mortari*, John R Hermanson, Elizabeth Taras, O Douglas Wangensteen, Jonathan S Serody, and Bruce R Blazar Department of Pediatrics, Division of Hematology, Oncology and Blood and Marrow Transplant, University of Minnesota, Minneapolis, MN, USA Department of Physiology, University of Minnesota, Minneapolis, MN, USA Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA * Corresponding author; email: panos001{at}tc.umn.edu. IPS is a significant cause of morbidity and mortality post-BMT in humans. We have developed a murine IPS model in which pre-BMT conditioning (total body irradiation ± Cytoxan) and allogeneic T cells results in the recruitment of host monocytes and then donor T cells into the lung by day 7 post-BMT concomitant with development of severe lung dysfunction. Recently, we reported the T-dependent production of the T cell-attracting chemokine MIP-1 in the lungs of such recipient mice. We reasoned that MIP-1 might be a critical mediator of IPS. Lethally conditioned recipients were transplanted with MHC-disparate marrow and either wild type (MIP-1 +/+) or knockout (MIP-1-/-) spleen cells. Surprisingly, recipients of MIP-1-/- cells exhibited a decrease in specific compliance that appeared earlier (d3) than in recipients of MIP-1+/+ cells. Donor CD4+ as well as CD8+ T cell expansion also was increased at this time in the spleens of recipients of MIP-1-/- vs +/+ cells. Lungs of recipients of MIP-1-/- cells had earlier recruitment of both T cell subsets by day 3 post-BMT, concomitant with the influx of cells expressing the cytolysins granzymes A & B. Monocyte recruitment was not altered. Interestingly, levels of inflammatory cytokines were not increased and the T cell-attracting chemokines, MIP-1, RANTES and lymphotactin were decreased. The level of the anti-inflammatory cytokine IL-13 was lower in the serum and lungs of recipients of MIP-1-/- cells indicating a skewing towards a more inflammatory Th1 cytokine milieu. The unexpected findings indicate that donor-derived MIP-1 may play a role in fully allogeneic-induced IPS by limiting aggressive expansion of CD4+ and CD8+ T cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. A. Wysocki, Q. Jiang, A. Panoskaltsis-Mortari, P. A. Taylor, K. P. McKinnon, L. Su, B. R. Blazar, and J. S. 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L. Kirby, A. D. Luster, K. McKinnon, B. R. Blazar, and J. S. Serody Differential Roles for CCR5 Expression on Donor T Cells during Graft-versus-Host Disease Based on Pretransplant Conditioning J. Immunol., July 15, 2004; 173(2): 845 - 854. [Abstract] [Full Text] [PDF] A. Panoskaltsis-Mortari, A. Price, J. R. Hermanson, E. Taras, C. Lees, J. S. Serody, and B. R. Blazar In vivo imaging of graft-versus-host-disease in mice Blood, May 1, 2004; 103(9): 3590 - 3598. [Abstract] [Full Text] [PDF] G. C. Hildebrandt, U. A. Duffner, K. M. Olkiewicz, L. A. Corrion, N. E. Willmarth, D. L. Williams, S. G. Clouthier, C. M. Hogaboam, P. R. Reddy, B. B. Moore, et al. A critical role for CCR2/MCP-1 interactions in the development of idiopathic pneumonia syndrome after allogeneic bone marrow transplantation Blood, March 15, 2004; 103(6): 2417 - 2426. [Abstract] [Full Text] [PDF]

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