生物谷报道：来自布法罗大学的研究报告称：在骨降解和自身免疫疾病的炎症中有着重要地位的一个免疫系统组分（immune system component），在保护着口腔免受传染病病原体的侵害，而这种病原体却是人类牙周病（periodontal diseas）的主要诱因。
这个免疫系统组分是IL-17，在过去的18个月期间，被识别出在骨降解和自身免疫疾病的炎症中是主要诱导分子。针对IL-17或它的细胞受体的疗法日前正在不断开发出来。
但是，布法罗大学的一名生物学家却发现，与该分子在类风湿性关节炎中的行为不同，IL-17却“反其道而行之”地保护着口腔免受传染病病原体的侵害，如牙龈卟啉菌（Porphyromonas gingivalis），该病菌是人类牙周病的主要诱因。
该研究发表在5月期的《血液》（Blood）杂志上。
原始出处:
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
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
Abstract
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.
