Abstract
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.
Highlights
Dentoalveolar abscesses and disseminating infections of endodontic origin occur as sequellae of bacterial invasion of the dental pulp
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
Mice were subjected to dentoalveolar infection with a mixture of four common human endodontic pathogens, and were treated subcutaneously with neutralizing antibodies against mouse IL-1α, IL-1β, or both on days 0, 3, 6, 9 and 12 relative to infection, or received unreactive goat IgG as a control
Summary
Dentoalveolar abscesses and disseminating infections of endodontic origin occur as sequellae of bacterial invasion of the dental pulp. We showed that B-cell- but not T-cell-deficient mice were susceptible to abscess formation and sepsis, and that passively transferred antibody, primarily IgG, against infecting bacteria was protective.[3,4] Mice doubly deficient in P- and E-selectin and reduced phagocyte migration, had decreased ability to slow the progress of dentoalveolar infections.[5] animals treated with the immunomodulator poly-(1-6)beta-D-glucopyranosyl-(1-3)-beta-D-glucopyranose (PGG)-glucan, which enhances neutrophil production and priming, had greater infection resistance.[6] Taken together these data indicate that antibody-mediated bacterial opsonization, combined with efficient phagocytosis and killing of bacteria by neutrophils are critical elements for protection
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
