作者: Gustavo P Garlet , Cristina RB Cardoso , Ana P Campanelli , Thiago P Garlet , Mario J Avila-Campos
DOI: 10.1016/J.MICINF.2008.01.010
关键词: Aggregatibacter actinomycetemcomitans 、 Interferon gamma 、 Biology 、 Immunology 、 Proinflammatory cytokine 、 Microbiology 、 Cytokine 、 Aggregatibacter 、 Acute-phase protein 、 Chemokine 、 Myeloperoxidase 、 Infectious Diseases
摘要: Inflammatory immune reactions in response to periodontopathogens trigger periodontal destruction, but their role protect the host against infection remains unknown. Thus, we examined mechanisms by which IFN-gamma modulates outcome of Aggregatibacter actinomycetemcomitans-induced disease mice. Our results showed that deficient mice developed less severe periodontitis A. actinomycetemcomitans infection, characterized significant lower alveolar bone loss and inflammatory reaction. However, absence increased bacterial load tissues higher acute phase reaction, followed a disseminated death during course disease. Such impaired was found be associated with reduction levels cytokines chemokines number GR1+, F4/80+, CD4+ CD8+ leukocytes diseased periodontium In addition, both antimicrobial mediators myeloperoxidase inducible nitric oxide synthase were also reduced IFN-KO demonstrate for first time may lethal an immunocompromised host. involved mediated cell migration tissues, its essential control clarified.