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Interleukin-1 and estrogen protect against disseminating dentoalveolar infections 被引量:7

Interleukin-1 and estrogen protect against disseminating dentoalveolar infections
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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-la (IL-1a) and IL-1β. Surprisingly male but not female mice given anti-lL-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-lL-1 blockade inhibited IL-12, interferon y (IFNy) and IL-6 but not IL-IO expression in infrabony lesions, suggestive of a local anti-inflammatory response. There was greater infiltration of neutrophils and other inflammatory ceils into lesions in anti-lL-l-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. 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-la (IL-1a) and IL-1β. Surprisingly male but not female mice given anti-lL-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-lL-1 blockade inhibited IL-12, interferon y (IFNy) and IL-6 but not IL-IO expression in infrabony lesions, suggestive of a local anti-inflammatory response. There was greater infiltration of neutrophils and other inflammatory ceils into lesions in anti-lL-l-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.
机构地区 host-microbiome center
出处 《International Journal of Oral Science》 SCIE CAS CSCD 2017年第1期16-23,共8页 国际口腔科学杂志(英文版)
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)
关键词 CYTOKINES DENTOALVEOLAR disseminating infections ESTROGEN NEUTROPHILS cytokines dentoalveolar disseminating infections estrogen neutrophils
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