IL-10, But Not IL-4, Suppresses Infection-Stimulated Bone Resorption In Vivo
Periapical bone resorption occurs following infection of the dental pulp and is mediated mainly by IL-1alpha in the murine model. The production and activity of IL-1alpha is modulated by a network of regulatory cytokines, including those produced by Th1 (pro-inflammatory) and Th2 (anti-inflammatory)...
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Published in | The Journal of immunology (1950) Vol. 165; no. 7; pp. 3626 - 3630 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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United States
Am Assoc Immnol
01.10.2000
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Abstract | Periapical bone resorption occurs following infection of the dental pulp and is mediated mainly by IL-1alpha in the murine model. The production and activity of IL-1alpha is modulated by a network of regulatory cytokines, including those produced by Th1 (pro-inflammatory) and Th2 (anti-inflammatory) subset T cells. This study was designed to assess the functional role of the Th2-type cytokines IL-4 and IL-10 in infection-stimulated bone resorption in vivo. The dental pulps of the first molars were exposed and infected with a mixture of four common endodontic pathogens, and bone destruction was determined by micro-computed tomography at sacrifice on day 21. The results demonstrate that IL-10(-/-) mice had significantly greater infection-stimulated bone resorption in vivo compared with wild-type mice (p < 0.001), whereas IL-4(-/-) exhibited no increased resorption. IL-10(-/-) had markedly elevated IL-1alpha production within periapical inflammatory tissues (>10-fold) compared with wild type (p < 0.01), whereas IL-4(-/-) exhibited decreased IL-1alpha production (p < 0.05). IL-10 also suppressed IL-1alpha production by macrophages in a dose-dependent fashion in vitro, whereas IL-4 had weak and variable effects. We conclude that IL-10, but not IL-4, is an important endogenous suppressor of infection-stimulated bone resorption in vivo, likely acting via inhibition of IL-1alpha expression. |
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AbstractList | Abstract
Periapical bone resorption occurs following infection of the dental pulp and is mediated mainly by IL-1α in the murine model. The production and activity of IL-1α is modulated by a network of regulatory cytokines, including those produced by Th1 (pro-inflammatory) and Th2 (anti-inflammatory) subset T cells. This study was designed to assess the functional role of the Th2-type cytokines IL-4 and IL-10 in infection-stimulated bone resorption in vivo. The dental pulps of the first molars were exposed and infected with a mixture of four common endodontic pathogens, and bone destruction was determined by micro-computed tomography at sacrifice on day 21. The results demonstrate that IL-10−/− mice had significantly greater infection-stimulated bone resorption in vivo compared with wild-type mice (p < 0.001), whereas IL-4−/− exhibited no increased resorption. IL-10−/− had markedly elevated IL-1α production within periapical inflammatory tissues (>10-fold) compared with wild type (p < 0.01), whereas IL-4−/− exhibited decreased IL-1α production (p < 0.05). IL-10 also suppressed IL-1α production by macrophages in a dose-dependent fashion in vitro, whereas IL-4 had weak and variable effects. We conclude that IL-10, but not IL-4, is an important endogenous suppressor of infection-stimulated bone resorption in vivo, likely acting via inhibition of IL-1α expression. Periapical bone resorption occurs following infection of the dental pulp and is mediated mainly by IL-1alpha in the murine model. The production and activity of IL-1alpha is modulated by a network of regulatory cytokines, including those produced by Th1 (pro-inflammatory) and Th2 (anti-inflammatory) subset T cells. This study was designed to assess the functional role of the Th2-type cytokines IL-4 and IL-10 in infection-stimulated bone resorption in vivo. The dental pulps of the first molars were exposed and infected with a mixture of four common endodontic pathogens, and bone destruction was determined by micro-computed tomography at sacrifice on day 21. The results demonstrate that IL-10(-/-) mice had significantly greater infection-stimulated bone resorption in vivo compared with wild-type mice (p < 0.001), whereas IL-4(-/-) exhibited no increased resorption. IL-10(-/-) had markedly elevated IL-1alpha production within periapical inflammatory tissues (>10-fold) compared with wild type (p < 0.01), whereas IL-4(-/-) exhibited decreased IL-1alpha production (p < 0.05). IL-10 also suppressed IL-1alpha production by macrophages in a dose-dependent fashion in vitro, whereas IL-4 had weak and variable effects. We conclude that IL-10, but not IL-4, is an important endogenous suppressor of infection-stimulated bone resorption in vivo, likely acting via inhibition of IL-1alpha expression. Periapical bone resorption occurs following infection of the dental pulp and is mediated mainly by IL-1 alpha in the murine model. The production and activity of IL-1 alpha is modulated by a network of regulatory cytokines, including those produced by Th1 (pro-inflammatory) and Th2 (anti-inflammatory) subset T cells. This study was designed to assess the functional role of the Th2-type cytokines IL-4 and IL-10 in infection-stimulated bone resorption in vivo. The dental pulps of the first molars were exposed and infected with a mixture of four common endodontic pathogens, and bone destruction was determined by micro-computed tomography at sacrifice on day 21. The results demonstrate that IL-10 super(-/-) mice had significantly greater infection-stimulated bone resorption in vivo compared with wild-type mice (p < 0.001), whereas IL-4 super(-/-) exhibited no increased resorption. IL-10 super(-/-) had markedly elevated IL-1 alpha production within periapical inflammatory tissues (> 10-fold) compared with wild type (p < 0.01), whereas IL-4 super(-/-) exhibited decreased IL-1 alpha production (p < 0.05). IL-10 also suppressed IL-1 alpha production by macrophages in a dose-dependent fashion in vitro, whereas IL-4 had weak and variable effects. We conclude that IL-10, but not IL-4, is an important endogenous suppressor of infection-stimulated bone resorption in vivo, likely acting via inhibition of IL-1 alpha expression. Periapical bone resorption occurs following infection of the dental pulp and is mediated mainly by IL-1alpha in the murine model. The production and activity of IL-1alpha is modulated by a network of regulatory cytokines, including those produced by Th1 (pro-inflammatory) and Th2 (anti-inflammatory) subset T cells. This study was designed to assess the functional role of the Th2-type cytokines IL-4 and IL-10 in infection-stimulated bone resorption in vivo. The dental pulps of the first molars were exposed and infected with a mixture of four common endodontic pathogens, and bone destruction was determined by micro-computed tomography at sacrifice on day 21. The results demonstrate that IL-10(-/-) mice had significantly greater infection-stimulated bone resorption in vivo compared with wild-type mice (p < 0.001), whereas IL-4(-/-) exhibited no increased resorption. IL-10(-/-) had markedly elevated IL-1alpha production within periapical inflammatory tissues (>10-fold) compared with wild type (p < 0.01), whereas IL-4(-/-) exhibited decreased IL-1alpha production (p < 0.05). IL-10 also suppressed IL-1alpha production by macrophages in a dose-dependent fashion in vitro, whereas IL-4 had weak and variable effects. We conclude that IL-10, but not IL-4, is an important endogenous suppressor of infection-stimulated bone resorption in vivo, likely acting via inhibition of IL-1alpha expression. |
Author | Uchiyama, Toru Wang, Cun-Yu Stashenko, Philip Hou, Linda Belani, Anita Muller, Ralph Sasaki, Hajime |
Author_xml | – sequence: 1 fullname: Sasaki, Hajime – sequence: 2 fullname: Hou, Linda – sequence: 3 fullname: Belani, Anita – sequence: 4 fullname: Wang, Cun-Yu – sequence: 5 fullname: Uchiyama, Toru – sequence: 6 fullname: Muller, Ralph – sequence: 7 fullname: Stashenko, Philip |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/11034365$$D View this record in MEDLINE/PubMed |
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Snippet | Periapical bone resorption occurs following infection of the dental pulp and is mediated mainly by IL-1alpha in the murine model. The production and activity... Abstract Periapical bone resorption occurs following infection of the dental pulp and is mediated mainly by IL-1α in the murine model. The production and... Periapical bone resorption occurs following infection of the dental pulp and is mediated mainly by IL-1 alpha in the murine model. The production and activity... |
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SubjectTerms | Animals Bone Resorption - genetics Bone Resorption - immunology Bone Resorption - microbiology Bone Resorption - pathology Cells, Cultured Cytokines - biosynthesis Disease Models, Animal Gram-Negative Bacterial Infections - genetics Gram-Negative Bacterial Infections - immunology Gram-Negative Bacterial Infections - pathology Gram-Positive Bacterial Infections - genetics Gram-Positive Bacterial Infections - immunology Gram-Positive Bacterial Infections - pathology Immunosuppressive Agents - administration & dosage Interleukin 1^a Interleukin-1 - biosynthesis Interleukin-10 - administration & dosage Interleukin-10 - deficiency Interleukin-10 - genetics Interleukin-10 - physiology Interleukin-4 - administration & dosage Interleukin-4 - deficiency Interleukin-4 - genetics Interleukin-4 - physiology Macrophages, Peritoneal - immunology Macrophages, Peritoneal - metabolism Macrophages, Peritoneal - microbiology Male Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Knockout Periapical Periodontitis - genetics Periapical Periodontitis - immunology Periapical Periodontitis - microbiology Periapical Periodontitis - pathology |
Title | IL-10, But Not IL-4, Suppresses Infection-Stimulated Bone Resorption In Vivo |
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