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Interleukin-1 and estrogen protect against disseminating dentoalveolar infections

查看全文 作　　者：hesham [1]youssef;philip [1]stashenko 高影响力作者 机构地区：[1]host-microbiome center,department of applied oral sciences,the forsyth institute,Cambridge,USA高影响力机构 出　　处：《International Journal of Oral Science》索引2017年第9卷第1期,共8页高影响力期刊 基　　金：supported by grant DE-11664(PS)from the National Institute of Dental and Craniofacial Research/National Institutes of Health(NIDCR/NIH);a grant from the American Association of Endodontists(HY) 摘　　要：Dentoalveolar bacterial infections cause localized tissue and bone destruction, but usually remain well-localized within teeth in immunocompetent hosts. However, in certain cases these infections may invade head and neck tissues, resulting in orofacial abscesses, cellulitis and sepsis, with resultant high morbidity and even mortality. In the present studies, we developed a novel model of spreading dentoalveolar infections in mice by treatment with neutralizing antibodies against both interleukin-1α(IL-1α)and IL-1β. Surprisingly male but not female mice given anti-IL-1 antibodies developed orofacial abscesses, weight loss,splenomegaly and sepsis. Female mice developed abscesses and sepsis comparable to males following ovariectomy(OVX), which was reversed by estrogen supplementation. Anti-IL-1 blockade inhibited IL-12, interferon γ(IFNγ) and IL-6 but not IL-10 expression in infrabony lesions, suggestive of a local anti-inflammatory response. There was greater infiltration of neutrophils and other inflammatory cells into lesions in anti-IL-1-treated animals; however, blood leukocytes had reduced bacterial phagocytic and killing activity ex vivo. Estrogen directly stimulated IL-1 production by macrophages, suggesting that the resistance of females to disseminating dentoalveolar infections may be due to their heightened pro-inflammatory responses following bacterial challenge, leading to enhanced localization of these infections. 关 键 词：cytokines DENTOALVEOLAR disseminating infections ESTROGEN NEUTROPHILS
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