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This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Forlow, S. B. Articles by Ley, K. Search for Related Content PubMed PubMed Citation Articles by Forlow, S. B. Articles by Ley, K. Related Collections Hematopoiesis and Stem Cells Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 December 2001, Vol. 98, No. 12, pp. 3309-3314 HEMATOPOIESIS Increased granulopoiesis through interleukin-17 and granulocyte colony-stimulating factor in leukocyte adhesion molecule-deficient mice S. Bradley Forlow, Jill R. Schurr, Jay K. Kolls, Gregory J. Bagby, Paul O. Schwarzenberger, and Klaus Ley From the Department of Biomedical Engineering and Cardiovascular Research Center, University of Virginia School of Medicine, Charlottesville; and the Gene Therapy Program and Department of Physiology, Louisiana State University Health Sciences Center, New Orleans. Many mutant mice deficient in leukocyte adhesion molecules display altered hematopoiesis and neutrophilia. This study investigated whether peripheral blood neutrophil concentrations in these mice are elevated as a result of accumulation of neutrophils in the circulation or altered hematopoiesis mediated by a disrupted regulatory feedback loop. Chimeric mice were generated by transplanting various ratios of CD18+/+ and CD18/ unfractionated bone marrow cells into lethally irradiated wild-type mice, resulting in approximately 0%, 10%, 50%, 90%, or 100% CD18 null neutrophils in the blood. The presence of only 10% CD18+/+ neutrophils was sufficient to prevent the severe neutrophilia seen in mice reconstituted with CD18/ bone marrow cells. These data show that the neutrophilia in CD18/ mice is not caused by enhanced neutrophil survival or the inability of neutrophils to leave the vascular compartment. In CD18/, CD18/E/, CD18/P/, EP/, and EPI/ mice, levels of granulocyte colony-stimulating factor (G-CSF) and interleukin-17 (IL-17) were elevated in proportion to the neutrophilia seen in these mice, regardless of the underlying mutation. Antibiotic treatment or the propensity to develop skin lesions did not correlate with neutrophil counts. Blocking IL-17 or G-CSF function in vivo significantly reduced neutrophil counts in severely neutrophilic mice by approximately 50% (P < .05) or 70% (P < .01), respectively. These data show that peripheral blood neutrophil numbers are regulated by a feedback loop involving G-CSF and IL-17 and that this feedback loop is disrupted when neutrophils cannot migrate into peripheral tissues. © 2001 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: E. Smith, M. A. Stark, A. Zarbock, T. L. Burcin, A. C. Bruce, D. Vaswani, P. Foley, and K. Ley IL-17A Inhibits the Expansion of IL-17A-Producing T Cells in Mice through "Short-Loop" Inhibition via IL-17 Receptor J. Immunol., July 15, 2008; 181(2): 1357 - 1364. [Abstract] [Full Text] [PDF] X. Cullere, M. Lauterbach, N. Tsuboi, and T. N. Mayadas Neutrophil-selective CD18 silencing using RNA interference in vivo Blood, April 1, 2008; 111(7): 3591 - 3598. [Abstract] [Full Text] [PDF] E. Smith, A. Zarbock, M. A. Stark, T. L. Burcin, A. C. Bruce, P. Foley, and K. 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