SEARCH:   Advanced

Blood, 1 May 2007, Vol. 109, No. 9, pp. 3794-3802. Prepublished online as a Blood First Edition Paper on January 3, 2007; DOI 10.1182/blood-2005-09-010116. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2005-09-010116v1 109/9/3794    most recent 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 Yu, J. J. Articles by Gaffen, S. L. Search for Related Content PubMed PubMed Citation Articles by Yu, J. J. Articles by Gaffen, S. L. Related Collections Immunobiology Phagocytes Signal Transduction Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY An essential role for IL-17 in preventing pathogen-initiated bone destruction: recruitment of neutrophils to inflamed bone requires IL-17 receptor–dependent signals Jeffrey J. Yu1, Matthew J. Ruddy1, Grace C. Wong2, Cornelia Sfintescu2, Pamela J. Baker3, Jeffrey B. Smith4, Richard T. Evans2, and Sarah L. Gaffen1,2 1 Department of Microbiology and Immunology, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), Buffalo, NY; 2 Department of Oral Biology, School of Dental Medicine, University at Buffalo, SUNY, Buffalo NY; 3 Department of Biology, Bates College, Lewiston ME; 4 Department of Pediatrics, David Geffen School of Medicine and Mattel Children's Hospital at University of California at Los Angeles, Los Angeles, CA IL-17 and its receptor are founding members of a novel family of inflammatory cytokines. IL-17 plays a pathogenic role in rheumatoid arthritis (RA)–associated bone destruction. However, IL-17 is also an important regulator of host defense through granulopoiesis and neutrophil trafficking. Therefore, the role of IL-17 in pathogen-initiated bone loss was not obvious. The most common form of infection-induced bone destruction occurs in periodontal disease (PD). In addition to causing significant morbidity, PD is a risk factor for atherosclerotic heart disease and chronic obstructive pulmonary disease (COPD). Similar to RA, bone destruction in PD is caused by the immune response. However, neutrophils provide critical antimicrobial defense against periodontal organisms. Since IL-17 is bone destructive in RA but a key regulator of neutrophils, we examined its role in inflammatory bone loss induced by the oral pathogen Porphyromonas gingivalis in IL-17RA–deficient mice. These mice showed enhanced periodontal bone destruction, suggesting a bone-protective role for IL-17, reminiscent of a neutrophil deficiency. Although IL-17RA–deficient neutrophils functioned normally ex vivo, IL-17RA knock-out (IL-17RAKO) mice exhibited reduced serum chemokine levels and concomitantly reduced neutrophil migration to bone. Consistently, CXCR2KO mice were highly susceptible to alveolar bone loss; interestingly, these mice also suggested a role for chemokines in maintaining normal bone homeostasis. These results indicate a nonredundant role for IL-17 in mediating host defense via neutrophil mobilization. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: H. Sasaki, N. Suzuki, R. Kent Jr., N. Kawashima, J. Takeda, and P. Stashenko T Cell Response Mediated by Myeloid Cell-Derived IL-12 Is Responsible for Porphyromonas gingivalis-Induced Periodontitis in IL-10-Deficient Mice J. Immunol., May 1, 2008; 180(9): 6193 - 6198. [Abstract] [Full Text] [PDF] G. Hajishengallis, M.-A. K. Shakhatreh, M. Wang, and S. Liang Complement Receptor 3 Blockade Promotes IL-12-Mediated Clearance of Porphyromonas gingivalis and Negates Its Virulence In Vivo J. Immunol., August 15, 2007; 179(4): 2359 - 2367. [Abstract] [Full Text] [PDF]

	Copyright © 2007 by American Society of Hematology         Online ISSN: 1528-0020