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曼氏血吸虫病小鼠模型中的肉芽肿存在生长抑素免疫调节回路。

Granulomas in murine schistosomiasis mansoni have a somatostatin immunoregulatory circuit.

作者信息

Elliott D E, Weinstock J V

机构信息

Department of Medicine, University of Iowa, Iowa City 52242, USA.

出版信息

Metabolism. 1996 Aug;45(8 Suppl 1):88-90. doi: 10.1016/s0026-0495(96)90093-1.

DOI:10.1016/s0026-0495(96)90093-1
PMID:8769393
Abstract

The role of somatostatin (SRIF) in controlling the granulomatous inflammatory response to infection with the parasite Schistosoma mansoni was explored in mice. The murine granulomas contain SRIF-14. Immunoreactive SRIF and prepro SRIF localize in the cytoplasmic granules of macrophages within the granulomas. The granulomas contain mRNA for prepro SRIF and are not innervated. The production of SRIF by the inflammatory cells appears to be inducible. The granulomas contain mRNA for the SRIF receptors sst2A and sst2B, which are expressed mainly on CD4- T lymphocytes and bind SRIF-14 with high affinity. Antigens from the schistosome eggs stimulate granuloma T lymphocytes to produce cytokines. Interferon-gamma (IFN-gamma) is one such cytokine made by CD4+ T lymphocytes. SRIF-14 suppresses antigen-induced IFN-gamma production from granuloma cells, and this effect is blocked by anti-sst2 antibody. SRIF was shown to inhibit IFN-gamma-induced immunoglobulin G2a (lgG2a) synthesis in murine schistosomiasis. SRIF also blocks substance P (SP)-stimulated IFN-gamma and lgG2a secretion. Schistosome-infected animals treated with the SRIF analog octreotide form smaller granulomas that secrete substantially less IFN-gamma and lgG2a. Unpublished observations suggest that SRIF does not modulate schistosome egg antigen- or concanavalin A-stimulated granuloma lymphocyte proliferation in murine schistosomiasis. In conclusion, SRIF may be an important factor in the control of the granulomatous inflammatory response in murine schistosomiasis.

摘要

在小鼠中探究了生长抑素(SRIF)在控制对曼氏血吸虫感染的肉芽肿性炎症反应中的作用。鼠类肉芽肿含有SRIF - 14。免疫反应性SRIF和前体SRIF定位于肉芽肿内巨噬细胞的细胞质颗粒中。肉芽肿含有前体SRIF的mRNA且无神经支配。炎症细胞产生SRIF的过程似乎是可诱导的。肉芽肿含有SRIF受体sst2A和sst2B的mRNA,它们主要在CD4⁺ T淋巴细胞上表达,并与SRIF - 14高亲和力结合。血吸虫卵抗原刺激肉芽肿T淋巴细胞产生细胞因子。干扰素 - γ(IFN - γ)是CD4⁺ T淋巴细胞产生的一种此类细胞因子。SRIF - 14抑制抗原诱导的肉芽肿细胞产生IFN - γ,且这种作用被抗sst2抗体阻断。已证明SRIF在小鼠血吸虫病中抑制IFN - γ诱导的免疫球蛋白G2a(IgG2a)合成。SRIF还阻断P物质(SP)刺激的IFN - γ和IgG2a分泌。用SRIF类似物奥曲肽治疗的血吸虫感染动物形成较小的肉芽肿,分泌的IFN - γ和IgG2a显著减少。未发表的观察结果表明,在小鼠血吸虫病中,SRIF不调节血吸虫卵抗原或伴刀豆球蛋白A刺激的肉芽肿淋巴细胞增殖。总之,SRIF可能是控制小鼠血吸虫病肉芽肿性炎症反应的一个重要因素。

相似文献

1
Granulomas in murine schistosomiasis mansoni have a somatostatin immunoregulatory circuit.曼氏血吸虫病小鼠模型中的肉芽肿存在生长抑素免疫调节回路。
Metabolism. 1996 Aug;45(8 Suppl 1):88-90. doi: 10.1016/s0026-0495(96)90093-1.
2
Substance P and somatostatin can modulate the amount of IgG2a secreted in response to schistosome egg antigens in murine schistosomiasis mansoni.P物质和生长抑素可调节曼氏血吸虫病小鼠体内针对血吸虫卵抗原分泌的IgG2a量。
J Immunol. 1993 Dec 15;151(12):6994-7004.
3
Granuloma T lymphocytes in murine schistosomiasis mansoni have somatostatin receptors and respond to somatostatin with decreased IFN-gamma secretion.曼氏血吸虫病小鼠中的肉芽肿T淋巴细胞具有生长抑素受体,且对生长抑素作出反应,分泌的γ干扰素减少。
J Immunol. 1992 Dec 1;149(11):3621-6.
4
The substance P and somatostatin interferon-gamma immunoregulatory circuit.P物质与生长抑素-γ干扰素免疫调节回路。
Ann N Y Acad Sci. 1998 May 1;840:532-9. doi: 10.1111/j.1749-6632.1998.tb09592.x.
5
Substance P modulates antigen-induced, IFN-gamma production in murine Schistosomiasis mansoni.P物质调节曼氏血吸虫病小鼠模型中抗原诱导的γ干扰素产生。
J Immunol. 1993 Jul 1;151(1):225-33.
6
T lymphocytes isolated from the hepatic granulomas of schistosome-infected mice express somatostatin receptor subtype II (SSTR2) messenger RNA.从感染血吸虫的小鼠肝脏肉芽肿中分离出的T淋巴细胞表达生长抑素受体II型(SSTR2)信使核糖核酸。
J Immunol. 1994 Aug 1;153(3):1180-6.
7
The role of cytokines in the formation of the schistosome egg granuloma.细胞因子在血吸虫虫卵肉芽肿形成中的作用。
Immunobiology. 1994 Oct;191(4-5):441-50. doi: 10.1016/S0171-2985(11)80450-X.
8
Schistosoma mansoni egg-induced hepatic granulomas in mice deficient for the interferon-gamma receptor have altered populations of macrophages, lymphocytes and connective tissue cells.曼氏血吸虫卵诱导的γ-干扰素受体缺陷小鼠的肝肉芽肿中,巨噬细胞、淋巴细胞和结缔组织细胞群体发生了改变。
Microbes Infect. 2000 Dec;2(15):1817-26. doi: 10.1016/s1286-4579(00)01341-1.
9
Substance P regulates somatostatin expression in inflammation.P物质在炎症中调节生长抑素的表达。
J Immunol. 1998 Dec 1;161(11):6316-22.
10
Modulation of T lymphocyte proliferation in mice infected with Schistosoma mansoni: VIP suppresses mitogen- and antigen-induced T cell proliferation possibly by inhibiting IL-2 production.曼氏血吸虫感染小鼠中T淋巴细胞增殖的调节:血管活性肠肽可能通过抑制白细胞介素-2的产生来抑制丝裂原和抗原诱导的T细胞增殖。
Cell Immunol. 1993 Jun;149(1):11-23. doi: 10.1006/cimm.1993.1132.

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Biomed Res Int. 2014;2014:247182. doi: 10.1155/2014/247182. Epub 2014 Jul 9.
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Somatostatin in inflammatory bowel disease.炎症性肠病中的生长抑素。
Mediators Inflamm. 1997;6(5-6):303-9. doi: 10.1080/09629359791424.
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Sequential expression of the neuropeptides substance P and somatostatin in granulomas associated with murine cysticercosis.神经肽P物质和生长抑素在小鼠囊尾蚴病相关肉芽肿中的顺序表达。
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Somatostatin does not attenuate intestinal injury in dextran sodium sulphate-induced subacute colitis.生长抑素不能减轻葡聚糖硫酸钠诱导的亚急性结肠炎中的肠道损伤。
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