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Deficiency of the macrophage migration inhibitory factor gene has no significant effect on endotoxaemia

IMMUNOLOGY 2000年第1期100卷 84-90页

作者： Honma, N Koseki, H Akasaka, T Nakayama, T Taniguchi, M Serizawa, I Akahori, H Osawa, M Mikayama, T Kirin Brewery Co Ltd Pharmaceut Res Lab Gunma Japan Chiba Univ Grad Sch Med Dept Mol Immunol Chiba Japan Chiba Univ Grad Sch Med Dept Mol Embryol Chiba Japan

By targeted disruption of the MIF gene, we have established a mouse strain deficient in macrophage (M phi) migration inhibitory factor (MIF). Despite previous reports indicating an essential role of MIF in endotoxaemia, an injection of lipopolysaccharide (LPS) into the MIF-deficient mice (maintained under specific pathogen-free conditions) caused shock. No significant difference was detected between the MIF-deficient mutant and normal mice in susceptibility to LPS for endotoxaemia or tumour necrosis factor-alpha (TNF-alpha) formation upon LPS injection. Peritoneal M phi from the two strains produced TNF-alpha in response to LPS with similar dose responses. Dexamethasone suppressed the LPS-induced TNF-alpha response of M phi, but no difference was detected between the M phi from the two strains. These results suggest that endogenous MIF has no significant effect on the LPS-induced TNF-alpha production and no effect on suppression of the response by glucocorticoids. Thus, MIF is not crucial for LPS-induced immune responses leading to shock.

关键词：消炎药/药理学地塞米松/药理学内毒素血症/免疫学生育力脂多糖类/免疫学巨噬细胞活化/药物作用巨噬细胞活化/免疫学巨噬细胞游走抑制因子/缺乏巨噬细胞游走抑制因子/遗传学巨噬细胞游走抑制因子/免疫学巨噬细胞腹膜/免疫学小鼠基因敲除休克脓毒性/免疫学存活率肿瘤坏死因子α/生物合成动物小鼠

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In vitro T-cell activation of monocyte-derived macrophages by soluble messengers or cell-to-cell contact in bovine tuberculosis

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IMMUNOLOGY 2000年第2期100卷 194-202页

作者： Liébana, E Aranaz, A Welsh, M Neill, SD Pollock, JM Dept Agr No Ireland Vet Sci Div Belfast BT4 3SD Antrim North Ireland Queens Univ Belfast Dept Vet Sci Belfast Antrim North Ireland

The macrophage plays a dual role in tuberculosis, promoting not only protection against mycobacteria, but also survival of the pathogen. Macrophages inhibit multiplication of mycobacteria but also act in concert with lymphocytes through presentation of antigens to T cells. Studies in animal and human infections have suggested a correlation of in vitro growth rates of mycobacteria with in vivo virulence, using uracil uptake to assess mycobacterial metabolism. This study found that blood-derived, non-activated bovine macrophages were capable of controlling Mycobacterium bovis bacillus Calmette-Guerin growth for up to 96 hr, but were permissive to intracellular growth of virulent M. bovis. The present investigation compared the in vitro modulation of these macrophage activities by cytokine-rich T-cell supernatants or cell-to-cell contact. On the one hand, treatment of cultured monocytes with mitogen-produced T-cell supernatants promoted morphological changes suggestive of an activation status, enhanced the antigen presentation capabilities of monocytes and up-regulated major histocompatibility complex class II expression. However, this activation was not associated with enhanced anti-M. bovis activity. On the other hand, incubation of infected monocytes with T-cell populations resulted in proportionally increased inhibition of M. bovis uracil uptake. This inhibition was also seen using cells from uninfected animals and indicated the necessity for cell-to-cell contact to promote antimycobacterial capability.

关键词：抗原呈递/免疫学细胞间通讯/免疫学细胞培养技术细胞分裂/免疫学培养基条件性组织相容性抗原Ⅱ类/代谢巨噬细胞活化/免疫学巨噬细胞/微生物学单核细胞/细胞学单核细胞/免疫学牛分枝杆菌/生长和发育溶解度 T淋巴细胞/免疫学结核牛/免疫学增量调节/免疫学动物牛男(雄)性

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Pseudoexons and regulatory elements in the genomic sequence of the β-chemokine, alternative macrophage activation-associated CC-chemokine (AMAC)-1

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CYTOKINE 2000年第2期12卷 120-126页

作者： Politz, O Kodelja, V Guillot, P Orfanos, CE Goerdt, S Free Univ Berlin Klinikum Benjamin Franklin Dermatol Klin & Poliklin D-12200 Berlin Germany

Recently, the authors reported the cloning of a novel human CC chemokine of alternatively activated macrophages (AMAC-1), whose expression is induced by Th2-associated cytokines such as interleukin 4 (IL-4), IL-13 and IL-10;vice versa, AMAC-1 expression is inhibited by Th1-associated cytokines such as interferon gamma (IFN-gamma), In order to study the genomic organization and transcriptional regulation of the AMAC-1 gene, genomic clones were isolated by screening a human lambda genomic library. Sequencing of a clone with a 1.7-kb insert gave a partial genomic sequence for the AMAC-1 gene. The complete AMAC-1 genomic sequence was obtained by bioinformational methods and the whole region spanning the AMAC-1 gene was verified by PCR amplification of subfragments and sequencing. The AMAC-1 gene consists of three exons, Whereas exons 2 and 3 were separated by a small intron of 411 bp, exon 1 and exon 2 were separated by 6 kb of non-translated genomic sequence containing two pseudoexons that are not expressed although they feature intact exon/intron boundaries and complete open reading frames. In order to allow a detailed analysis, a 2.7-kb fragment containing the promoter region and the first exon of AMAC-1 gene was cloned into a reporter gene construct. In the AMAC-1 promoter, two possible transcription start points were identified. In addition, several putative regulatory sequences for IL-4- and IFN-gamma-dependent transcriptional pathways mere found including STAT6 and STAT1 binding sites as well as several AP-1 and C/EBP elements. Interestingly, a combined STAT6/STAT1 binding element is located in the direct vicinity of the first putative transcription start point. Competitive binding of IL-4-induced STAT6 versus IFN-gamma-induced STAT1 to this site may explain the antagonistic effects these cytokines exert on AMAC-1 expression. (C) 2000 Academic Press.

关键词：氨基酸序列碱基序列趋化因子 CC/遗传学克隆分子共有序列 DNA/遗传学 DNA引物/遗传学外显子基因调节基因组文库内含子巨噬细胞活化/遗传学巨噬细胞活化/免疫学分子序列数据启动区(遗传学) 序列同源性核酸人类

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The role of immunostimulatory CpG-DNA in septic shock

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SPRINGER SEMINARS IN IMMUNOPATHOLOGY 2000年第1-2期22卷 167-171页

作者： Wagner, H Lipford, GB Häcker, H Tech Univ Munich Inst Med Microbiol Immunol & Hyg D-81675 Munich Germany

Studies the role of immunostimulatory CpG-DNA in septic shock. Evolutionary vestige of foreign DNA; Signal pathway for cell activation; Methylation of bacterial DNA.

关键词：佐剂免疫细菌毒素类/免疫学 CpG岛/免疫学细胞因子类/生理学 DNA 细菌/免疫学树突细胞/免疫学进化分子 HLA-D抗原/免疫学白细胞介素1/生理学脂多糖类/免疫学巨噬细胞活化/免疫学受体抗原 T细胞/免疫学休克脓毒性/免疫学超抗原/免疫学肿瘤坏死因子α/生理学动物人类小鼠

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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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Serum neopterin and complex stenosis morphology in patients with unstable angina

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 2000年第4期35卷 956-962页

作者： Garcia-Moll, X Coccolo, F Cole, D Kaski, JC St George Hosp Sch Med Artery Dis Res Grp London SW17 0RE England

OBJECTIVES We sought to assess the relation between serum neopterin concentration and complex coronary artery stenosis in patients with unstable angina. BACKGROUND Monocyte activation is associated. with acute atheromatous plaque disruption and acute coronary syndromes. Angiographically demonstrated complex coronary stenosis is often an expression of plaque disruption. Increased serum concentration of neopterin, a pterydine derivative secreted by macrophages after stimulation by interferon-gamma, has been observed in patients with acute coronary syndromes as compared with control subjects and patients with stable angina pectoris. METHODS We studied 50 patients with unstable angina (32 men) who underwent coronary angiography after hospital admission. All coronary stenoses with greater than or equal to 30% diameter reduction were assessed and classified as "complex" (irregular or scalloped borders, ulceration or filling defects suggesting thrombi) or "smooth" (absence of complex features). Serum neopterin levels were assessed within 24 h of hospital admission using a commercially available immunoassay (enzyme-linked immunosorbent assay kit, IBL, Hamburg, Germany). RESULTS Thirty-nine patients were classified in Braunwald class IIIb, four in class IIb and seven in class Ib. The number of complex lesions per patient was 2.6 +/- 1.8 (mean SD). The mean neopterin concentration was 7.76 +/- 3.62 nmol/liter. A significant correlation was observed between neopterin serum concentration and the presence of complex coronary stenoses (r = 0.35, p = 0.015). Multiple regression analysis showed that serum neopterin (p < 0.0001) was independently associated with the number of complex lesions. Other variables associated with complex lesions were the number of vessels with greater than or equal to 75% stenosis (p < 0.0001), plasma creatinine (p = 0.003), triglycerides (p = 0.014) and a history of unstable angina (p = 0.032). CONCLUSIONS Serum neopterin concentration is associated with

关键词：心绞痛不稳定型/诊断心绞痛不稳定型/免疫学冠状血管造影术冠状动脉疾病/诊断冠状动脉疾病/免疫学巨噬细胞活化/免疫学新蝶呤/血液预后老年人女(雌)性人类男(雄)性中年人

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Macrophages and cutaneous inflammation

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NATURE BIOTECHNOLOGY 2000年第1期18卷 25-26页

作者： McCormick, TS Stevens, SR Kang, K Case Western Reserve Univ Cleveland OH 44106 USA

Macrophage infiltration is a hallmark of inflammation, especially in the skin. Although the macrophage response is generally a favorable event in the course of an infection, quite often macrophages can mediate chronic inflammation. This is seen in several inflammatory dermatoses including psoriasis, atopic dermatitis, and chronic contact dermatitis. Several lines of investigation have concentrated on limiting the macrophage response as a means of eliminating the inflammatory response. In this issue, Thepen and colleagues^1 have taken a more direct approach, targeting the macrophage itself for local apoptotic elimination, using an engineered immunotoxin. Taking advantage of the expression of the immunoglobulin receptor FcγRI, and its upregulation on macrophages during inflammation, this team used a monoclonal antibody against the receptor to which they conjugated the Ricin-A toxin. This immunotoxin was shown to induce apoptosis in macrophages that are participating in a chronic inflammatory response in the skin. They further demonstrated that clearance of the inflammatory macrophages led to the diminution of both T cells and dendritic cells, thus allowing the inflammation to become quiescent.

关键词：细胞凋亡慢性病细胞因子类/生理学皮炎/药物疗法皮炎/免疫学皮炎/病理学免疫毒素类/免疫学免疫毒素类/代谢免疫毒素类/治疗应用巨噬细胞活化/免疫学巨噬细胞/细胞学巨噬细胞/药物作用巨噬细胞/免疫学受体 Fc/免疫学蓖麻蛋白皮肤/药物作用皮肤/免疫学皮肤/病理学皮肤疾病/免疫学皮肤疾病/病理学动物人类

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Activation of macrophage cytostatic effector mechanisms during acute graft-versus-host disease: release of intracellular iron and nitric oxide-mediated cytostasis

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BLOOD 2000年第5期96卷 1836-1843页

作者： Nestel, FP Greene, RN Kichian, K Ponka, P Lapp, WS McGill Univ Dept Physiol Montreal PQ H3G 1Y6 Canada Sir Mortimer B Davis Jewish Gen Hosp Lady Davis Inst Med Res Montreal PQ H3T 1E2 Canada

During acute graft-versus-host disease (GVHD) the activation of macrophages (M phi) is mediated by 2 signals, interferon (IFN)-gamma and bacteria-derived lipopolysaccharide (LPS). A cascade of inflammatory responses that includes the release of mediators of tissue injury follows M phi activation. Among the tissues characteristically targeted during acute GVHD are epithelial tissues of the skin and gastrointestinal tract that normally undergo continuous proliferation and are therefore sensitive to cytostatic processes. We have investigated whether M phi can mediate cytostatic mechanisms capable of interrupting cell proliferation during acute GVHD. GVHD was induced in nonirradiated C57BL/6XAF(1) (B6AF(1)) mice by the injection of 60 x 10(6) (acute GVHD) or 30 x 10(6) (nonlethal GVHD) C57BL/6 (B6) lymphoid cells. M phi from animals undergoing acute GVHD could be triggered by normally insignificant quantities of LPS to mediate a cytostatic effect on target cells, resulting in the complete shutdown of cellular proliferation. The same amounts of LPS had no effect on M phi from normal or syngeneically transplanted animals. M phi mediated the release of significant quantities of intracellular iron from target cells undergoing cytostasis. Reversal of cytostasis occurred following inhibition of nitric oxide (NO) production by NG-monomethyl-l-arginine (NMMA). Production of NO by LPS-triggered M phi reflected the severity of GVHD, NO release increased significantly during acute GVHD but was only transiently increased during nonlethal GVHD. The results provide evidence that, as a result of activation during acute GVHD, M phi produce NO and induce the release of iron from target cells, resulting in a potent cytostatic effect that inhibits cellular proliferation. (C) 2000 by The American Society of Hematology.

关键词：急性病细胞分裂/药物作用细胞系共同培养技术细胞毒性免疫剂量效应关系药物移植物抗宿主病/代谢移植物抗宿主病/病理学干扰素Ⅱ型/药理学铁/代谢脂多糖类/药理学巨噬细胞活化/药物作用巨噬细胞活化/免疫学巨噬细胞/细胞学巨噬细胞/药物作用巨噬细胞/代谢小鼠近交C57BL 小鼠近交系一氧化氮/代谢疾病严重程度指数时间因素肿瘤细胞培养的 ωN-甲基精氨酸/药理学动物女(雌)性人类男(雄)性小鼠

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