共查询到20条相似文献,搜索用时 0 毫秒
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Pascal V Nathan NR Claudio E Siebenlist U Anderson SK 《Journal of immunology (Baltimore, Md. : 1950)》2007,179(3):1751-1759
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Mattioli I Sebald A Bucher C Charles RP Nakano H Doi T Kracht M Schmitz ML 《Journal of immunology (Baltimore, Md. : 1950)》2004,172(10):6336-6344
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NF-kappa B/Rel participation in the lymphokine-dependent proliferation of T lymphoid cells 总被引:2,自引:0,他引:2
Mora A Youn J Keegan A Boothby M 《Journal of immunology (Baltimore, Md. : 1950)》2001,166(4):2218-2227
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Gadjeva M Tomczak MF Zhang M Wang YY Dull K Rogers AB Erdman SE Fox JG Carroll M Horwitz BH 《Journal of immunology (Baltimore, Md. : 1950)》2004,173(9):5786-5793
To evaluate the possibility that NF-kappaB subunits p50 and p65 have a role in limiting the systemic inflammatory response induced by endotoxin, we compared the susceptibility of wild-type (WT), p65+/-, p50-/-, and p50-/-p65+/- (3X) mice to LPS-induced shock. Interestingly, whereas p65+/- mice were no more sensitive than WT mice to LPS-induced shock, 3X mice were exquisitely sensitive to the toxic effects of LPS. Mice lacking p50 alone displayed an intermediate phenotype. Sensitivity to LPS was a property of the innate immune system and was characterized by elevated circulating levels of TNF in both p50-/- and 3X mice. The ability of LPS to induce shock depended upon TNF, and 3X mice were significantly more sensitive to the toxic effects of TNF than were p50-deficient mice. The expression of several LPS-inducible proinflammatory genes, including IFN-gamma, was significantly higher within the spleens of p50-/- mice than in the spleens of WT mice, and interestingly, the expression of IFN-gamma was augmented still further within the spleens of 3X mice. These results demonstrate that NF-kappaB subunits p50 and p65 have critical inhibitory functions during the systemic response to LPS and raise the possibility that these functions could be essential in preventing mortality associated with systemic inflammatory response syndromes. 相似文献
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D'Angio CT LoMonaco MB Johnston CJ Reed CK Finkelstein JN 《American journal of physiology. Lung cellular and molecular physiology》2004,286(1):L30-L36
The alveolar macrophage is an important source of interleukin (IL)-8 during pulmonary injury. The IL-8 gene promoter sequence contains nuclear factor (NF)-kappa B, NF-IL6, and activator protein (AP)-1 binding sequences. These sites may have differing regulatory roles in hyperoxia-exposed macrophages than in those stimulated by bacterial lipopolysaccharide (LPS). U-937 and THP-1 macrophage-like cells were exposed to air-5% CO2 or 95% O2-5% CO2, with or without 1.0 microg/ml of LPS, and transfected with an IL-8 promoter-reporter containing NF-kappa B, NF-IL6, or AP-1 mutations. Hyperoxia and LPS caused additive increases in IL-8 production by U-937 cells, whereas THP-1 cells responded only to LPS. An NF-kappa B mutation ablated baseline and O2- and LPS-stimulated reporter activity in both cell lines, whereas NF-IL6 mutations had little effect. An AP-1 mutation had an intermediate effect. LPS, but not hyperoxia, stimulated nuclear translocation of NF-kappa B in both cell lines. Pharmacological blockade of NF-kappa B nuclear translocation ablated LPS-, but not hyperoxia-, stimulated IL-8 production. Although an intact promoter NF-kappa B site is crucial to macrophage IL-8 production, only LPS-stimulated production appears to require additional nuclear translocation of NF-kappa B. 相似文献
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