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IL-10 is necessary for the expression of airway hyperresponsiveness but not pulmonary inflammation after allergic sensitization

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第11期97卷 6007-6012页

作者： Mäkelä, MJ Kanehiro, A Borish, L Dakhama, A Loader, J Joetham, A Xing, Z Jordana, M Larsen, GL Gelfand, EW Natl Jewish Med & Res Ctr Dept Pediat Denver CO 80206 USA Natl Jewish Med & Res Ctr Dept Med Denver CO 80206 USA McMaster Univ Dept Mol Med Hamilton ON L8N 3Z5 Canada

Cytokines play an important role in modulating inflammatory responses and, as a result, airway tone. IL-10 is a regulatory cytokine that has been suggested for treatment of asthma because of its immunosuppressive and anti-inflammatory properties. In contrast to these suggestions, we demonstrate in a model of allergic sensitization that mice deficient in IL-10 (IL-10-/-) develop a pulmonary inflammatory response but fail to exhibit airway hyperresponsiveness in both in vitro and in vivo assessments of lung function. Reconstitution of these deficient mice with the IL-10 gene fully restores development of airway hyperresponsiveness comparable to control mice, These results identify an important role of IL-10, downstream of the inflammatory cascade, in regulating the tone of the airways after allergic sensitization and challenge.

关键词：气雾剂血蛋白质类/分析支气管高反应性/病理生理学支气管激发试验支气管肺泡灌洗液/化学细胞因子类/分析电刺激嗜酸细胞颗粒蛋白质类嗜酸细胞过氧化物酶嗜酸粒细胞增多/病因学嗜酸粒细胞增多/病理生理学基因疗法遗传互补测验免疫法炎症/病理生理学白细胞介素10/缺乏白细胞介素10/遗传学白细胞介素10/生理学白三烯类/分析肺/化学肺/病理学氯醋甲胆碱/投药和剂量氯醋甲胆碱/诊断应用小鼠近交C57BL 小鼠基因敲除肌平滑/病理生理学卵白蛋白/投药和剂量卵白蛋白/免疫学过氧化物酶类/分析呼吸超敏反应/病理生理学核糖核酸酶类无特异性病原体有机物气管/病理生理学动物女(雌)性男(雄)性小鼠

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Increased resistance to mycobacterial infection in the absence of interleukin-10

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IMMUNOLOGY 2000年第4期100卷 494-501页

作者： Jacobs, M Brown, N Allie, N Gulert, R Ryffel, B Univ Cape Town Dept Immunol ZA-7700 Rondebosch South Africa Univ Geneva Dept Pathol CH-1211 Geneva 4 Switzerland

Interleukin-10 (IL-10) down-regulates T helper type 1 cell and macrophage functions. As IL-10 is induced along with tumour necrosis factor (TNF) and IL-12 in mycobacterial infection, we asked whether endogenous IL-10 plays a role in the antimycobacterial response. We demonstrate here that IL-10-deficient mice eliminate Mycobacterium bovis Calmette-Guerin bacillus faster than wild-type mice. Granulomas are significantly larger, containing more CD-11b- and CD11c-positive antigen-presenting cells and T cells, and the expression of major histocompatibility complex class II and intracellular adhesion molecule-1 is increased. Macrophages in granulomas of IL-10-deficient mice express high levels of TNF, acid phosphatase and inducible nitric oxide synthase (iNOS). Finally, an increased cutaneous delayed-type hypersensitivity reaction to mycobacterial proteins is further evidence of an augmented cell-mediated immune response. In conclusion, the cell-mediated immunity is enhanced in the absence of IL-10, resulting in a robust granuloma response, which accelerates the clearance of mycobacteria. Therefore, endogenous IL-10 attenuates mycobacterial immunity.

关键词：细胞因子类/生物合成肉芽肿/免疫学超敏反应迟发型/免疫学免疫细胞/免疫学白细胞介素10/缺乏白细胞介素10/免疫学巨噬细胞活化/免疫学小鼠近交C57BL 牛分枝杆菌 T淋巴细胞/免疫学 Th1细胞/免疫学结核菌素/免疫学结核/免疫学动物女(雌)性小鼠

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Paralysis of dendritic cell IL-12 production by microbial products prevents infection-induced immunopathology

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IMMUNITY 1999年第5期11卷 637-647页

作者： Sousa, CRE Yap, G Schulz, O Rogers, N Schito, M Aliberti, J Hieny, S Sher, A Imperial Canc Res Fund Immunobiol Lab London WC2A 3PX England NIAID Immunobiol Sect Parasit Dis Lab NIH Bethesda MD 20892 USA

Interleukin-12 plays a major role in immunity to intracellular pathogens by governing the development of IFN gamma-dependent host resistance. Nevertheless, unregulated IL-12 synthesis can lead to immunopathology, an outcome prevented by the concurrent expression of interleukin-10. Dendritic cells (DC) are an important source of the initial IL-12 stimulated by microbial agents. Here, we show that, following systemic triggering, DC can no longer be restimulated to produce IL-12 in vivo while continuing to respond in vitro. When infected with Toxoplasma gondii during this refractory state, mice mount impaired acute IFN gamma responses and, in the case of IL-10-deficient animals, are protected from cytokine-induced mortality. These findings demonstrate a previously unrecognized form of immunologic paralysis involving DC that can protect from infection-induced immunopathology.

关键词：抗原原虫/免疫学抗原原虫/药理学细胞培养的树突细胞/药物作用树突细胞/免疫学树突细胞/代谢干扰素Ⅱ型/生物合成干扰素Ⅱ型/缺乏白细胞介素10/缺乏白细胞介素10/遗传学白细胞介素12/生物合成白细胞介素12/缺乏白细胞介素12/遗传学白细胞介素12/生理学小鼠近交C57BL 小鼠近交CBA 小鼠基因敲除模型免疫学脾/免疫学弓形虫属/免疫学弓形虫病动物/并发症弓形虫病动物/免疫学弓形虫病动物/病理学动物小鼠

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Increased tumor necrosis factor and interleukin-6 production in the central nervous system of interleukin-10-deficient mice

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BRAIN RESEARCH 2000年第1-2期869卷 241-243页

作者： Agnello, D Villa, P Ghezzi, P Mario Negri Inst Pharmacol Res Lab Neuroimmunol I-20157 Milan Italy CNR Cellular & Mol Pharmacol Ctr I-20129 Milan Italy

Interleukin-10 (IL-10) inhibits tumor necrosis factor (TNF) production. We investigated the role of endogenous IL-IO in brain TNF production. We injected IL-10-knockout mice with lipopolysaccharide (LPS,2.5 mu g/mouse i.c.v.). Brain TNF and IL-6 levels were more elevated and persisted longer in IL-10-deficient mice compared with wild type mice, suggesting that IL-10 is an important negative feedback inhibitor of TNF and IL-6 production in the CNS. (C) 2000 Elsevier Science BN. All rights reserved.

关键词：中枢神经系统/细胞学中枢神经系统/代谢白细胞介素10/缺乏白细胞介素6/代谢小鼠近交C57BL 小鼠基因敲除肿瘤坏死因子α/代谢动物男(雄)性小鼠

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Interleukin 10-deficient colitis: new similarities to human inflammatory bowel disease

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BRITISH JOURNAL OF SURGERY 2000年第10期87卷 1346-1351页

作者： Kennedy, RJ Hoper, M Deodhar, K Erwin, PJ Kirk, SJ Gardiner, KR Queens Univ Belfast Inst Clin Sci Dept Surg Belfast BT12 6BJ Antrim North Ireland Queens Univ Belfast Inst Clin Sci Dept Pathol Belfast BT12 6BJ Antrim North Ireland

Background: Interleukin (IL) 10 is a potent anti-inflammatory cytokine. Disruption of the IL-10 gene in C57/Black6 mice results in enterocolitis in the presence of intestinal bacteria. This study investigated gut mucosal barrier function sequentially during the development of colitis in this model. Methods: Animals were bred in specific pathogen-free conditions and transferred to conventional housing at 4 weeks. Mice were evaluated at 6, 8, 10, 12, 14 and 15 weeks of age. Barrier function was assessed by measuring intestinal permeability and antibody response to systemic endotoxaemia (antibody to the core glycolipid region of lipopolysaccharide;EndoCAb). Colons were harvested and a histological injury score (HIS) was calculated. Results: The HIS increased progressively until 12 weeks, with an associated increase in intestinal permeability, and immunoglobulin (Ig) M and IgG EndoCAb. The HIS correlated positively with both intestinal permeability and IgM and IgG EndoCAb. Intestinal permeability showed a positive correlation with EndoCAb. Conclusion: IL-10 knockout mice develop colitis with an associated disturbance in gut mucosal barrier function, as measured by increased permeability and endotoxaemia. The colitis found in the IL-10 knockout mouse shares these histological, physiological and biochemical features with human inflammatory bowel disease and is therefore suitable for therapeutic trials. A measure of endotoxaemia correlated directly with intestinal permeability in this model.

关键词：结肠炎/病因学结肠炎/病理学免疫球蛋白G/分析免疫球蛋白M/分析白细胞介素10/缺乏白细胞介素10/遗传学肠吸收肠黏膜/生理学小鼠近交C57BL 小鼠基因敲除动物小鼠

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Role of graft cytokine expression in the tolerogenicity of neonatal skin allografts

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TRANSPLANTATION PROCEEDINGS 1999年第1-2期31卷 813-813页

作者： Gozzo, J De Fazio, S Northeastern Univ Bouve Coll Pharm & Hlth Sci Boston MA 02115 USA

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