Journal of inflammation最新文献_第4页

Bidirectional feedback regulation on 17 kD tumor necrosis factor (TNF) production by 26 kD membrane-bound TNF precursor. 26kd膜结合肿瘤坏死因子前体对17kd肿瘤坏死因子(TNF)产生的双向反馈调节。

Journal of inflammation Pub Date : 1995-01-01

I G Soma, T Nishizawa, H Inagawa, Y Tanabe, K Noguchi, S Goto, K Takagi, D Mizuno

引用次数: 0

Identification of p55 tumor necrosis factor receptor-associated proteins that couple to signaling pathways not initiated by the death domain. p55肿瘤坏死因子受体相关蛋白与非死亡结构域信号通路偶联的鉴定

Journal of inflammation Pub Date : 1995-01-01

D Adam, S Adam-Klages, M Krönke

引用次数: 0

Dexamethasone downregulates lysosomal secretion in mouse macrophages: involvement of signaling through protein kinase C. 地塞米松下调小鼠巨噬细胞溶酶体分泌:通过蛋白激酶C参与信号传导。

Journal of inflammation Pub Date : 1995-01-01

K Gewert, H Tapper, C Nauclér, R Sundler

{"title":"Dexamethasone downregulates lysosomal secretion in mouse macrophages: involvement of signaling through protein kinase C.","authors":"K Gewert, H Tapper, C Nauclér, R Sundler","doi":"","DOIUrl":"","url":null,"abstract":"Spectrofluorimetric methods were used to investigate the effects of dexamethasone (dex) on cytosolic and lysosomal pH and on macrophage secretion of lysosomal contents. Secretion of N-acetyl-beta-D-glucosaminidase (NAG) in response to zymosan particles, lysosomotropic methylamine, or the H(+)-ATPase inhibitor bafilomycin A1 was inhibited by pretreatment with dex. The inhibition was not reversed by mannan and was seen also when secretion of preloaded fluorescein-labelled dextran was monitored, demonstrating that dex did not exert its effect by enhancing the reuptake of lysosomal enzyme. The binding of zymosan particles to macrophages was diminished after dex treatment, as was the zymosan-induced phospholipase C activation. However, the decreased binding of zymosan did not alone account for the inhibition of phospholipase C activation. Also, cytosolic pH was lowered by dex treatment. This might contribute to the inhibition of lysosomal secretion, but restoration of cytosolic pH by an increase in extracellular pH did not restore the secretory response. Lysosomal secretion induced by a combination of protein kinase C (PKC)-activating phorbol ester and methylamine was more resistant to dex than secretion induced by methylamine alone, or other secretagogues. We interpret this, together with previous data, to indicate that dex inhibits macrophage lysosomal secretion by attenuating one or more step(s) in a PKC-mediated signaling pathway necessary for the secretory response.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"47 3","pages":"115-25"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20065376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Absence of lymph nodes in lymphotoxin-alpha(LT alpha)-deficient mice is due to abnormal organ development, not defective lymphocyte migration. 淋巴xin- α (LT α)缺乏小鼠的淋巴结缺失是由于器官发育异常，而不是淋巴细胞迁移缺陷。

Journal of inflammation Pub Date : 1995-01-01

S Mariathasan, M Matsumoto, F Baranyay, M H Nahm, O Kanagawa, D D Chaplin

{"title":"Absence of lymph nodes in lymphotoxin-alpha(LT alpha)-deficient mice is due to abnormal organ development, not defective lymphocyte migration.","authors":"S Mariathasan, M Matsumoto, F Baranyay, M H Nahm, O Kanagawa, D D Chaplin","doi":"","DOIUrl":"","url":null,"abstract":"Mice homozygous for a targeted null mutation of lymphotoxin-alpha (LT alpha) are born without lymph nodes (LN) or Peyer's patches (PP) and with altered splenic architecture. To investigate the mechanism of failed LN organogenesis, we transferred bone marrow (BM) from Thy 1.2 LT alpha-deficient or Thy 1.2 wild type mice to lethally irradiated 8-12-week-old Thy 1.1 wild type recipients. Six to 10 weeks later, reconstitution of LN and spleen with Thy 1.2 cells was similar whether the BM was derived from LT alpha-deficient or wild type donors. In contrast, reconstitution of irradiated LT alpha-deficient mice with wild type BM did not induce the development of detectable LN, although reconstitution of the spleen occurred appropriately. The expression and regulation of the lymphocyte adhesion molecule L-selectin from the LT alpha-deficient mice appeared normal. These data indicate that LT alpha-dependent interactions must occur during development in order for LN genesis to take place; however, lymphocyte expression of LT alpha is not required for these cells to home to existing LN structures.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"45 1","pages":"72-8"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18588861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Interleukin-10 is upregulated in LPS tolerance. 白细胞介素-10在LPS耐受中上调。

Journal of inflammation Pub Date : 1995-01-01

M Frankenberger, H Pechumer, H W Ziegler-Heitbrock

{"title":"Interleukin-10 is upregulated in LPS tolerance.","authors":"M Frankenberger, H Pechumer, H W Ziegler-Heitbrock","doi":"","DOIUrl":"","url":null,"abstract":"Lipopolysaccharide (LPS) stimulation of the human monocytic cell line Mono Mac 6 leads to rapid expression of both the pro-inflammatory cytokine tumor necrosis factor (TNF) and the anti-inflammatory cytokine interleukin-10 (IL-10). Preculture of these cells with a low dose of LPS for 2 days rendered the cells tolerant to subsequent stimulation, in that TNF gene expression is only minimal, both at the mRNA and at the protein level. IL-10 shows a reciprocal pattern, however, as expression of this gene is upregulated in precultured cells, and it will further increase upon subsequent stimulation. Although TNF has been shown to induce IL-10, and IL-10 was found to downregulate TNF, this reciprocal regulation does not explain the pattern observed in LPS tolerance in Mono Mac 6, since neutralizing antibodies against TNF and IL-10 could not prevent upregulation of IL-10 and downregulation of TNF, respectively. Treatment of Mono Mac 6 cells during LPS preculture with interferon-gamma (IFN-gamma) could, however, reverse tolerance: LPS/IFN-gamma precultured cells produced high levels of TNF transcripts upon subsequent stimulation, while the response of the IL-10 gene was attenuated. The data show that LPS tolerance does not involve a passive downregulation of all types of monocyte functions, but it is an orchestrated response with downregulation of pro- and upregulation of anti-inflammatory cytokines.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"45 1","pages":"56-63"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18588859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Secretion of an anti-inflammatory, immunomodulatory factor by Schistosomulae of Schistosoma mansoni. 曼氏血吸虫分泌一种抗炎、免疫调节因子。

Journal of inflammation Pub Date : 1995-01-01

K Ramaswamy, B Salafsky, S Potluri, Y X He, J W Li, T Shibuya

{"title":"Secretion of an anti-inflammatory, immunomodulatory factor by Schistosomulae of Schistosoma mansoni.","authors":"K Ramaswamy, B Salafsky, S Potluri, Y X He, J W Li, T Shibuya","doi":"","DOIUrl":"","url":null,"abstract":"Penetration and migration of schistosomulae of Schistosoma mansoni through the skin of mice is associated with reduced inflammatory responses especially after a moderate infection. Previous studies to identify the mechanisms by which schistosomulae of S. mansoni suppress inflammatory responses in human skin showed that the excretory/secretory (ES) products of schistosomulae of s. mansoni contain activities that induce production of the antiinflammatory cytokine IL-1ra from human keratinocytes. In the present study we have characterized the ES products of the schistosomulae of S. mansoni to identify the IL-1ra inducing activity. We demonstrate that this anti-inflammatory activity is associated with a protein of molecular mass 16.8 kDa (Sm 16.8). Depletion studies confirm that Sm 16.8 is the major IL-1ra inducing activity in the ES products. A comparison of the proteins in the ES products of schistosomulae of S. mansoni with those of Trichobilharzia ocellata, a bird schistosome that induces an acute inflammation in human skin, shows that Sm 16.8 is absent in the ES products of T. ocellata. Interestingly, ES products of the schistosomulae of T. ocellata were potent inducers of IL-1 alpha from human keratinocytes, whereas ES products from schistosomulae of s. mansoni induce little or no IL-1 alpha secretion from keratinocytes. Functional studies show that Sm 16.8 suppresses antigen induced lymphoproliferative responses in vitro. Addition of Sm 16.8 to spleen or axillary lymph node cell cultures resulted in a significant reduction in antigen induced IL-2 secretion. These studies show that schistosomulae of S. mansoni elaborate an anti-inflammatory, immunomodulatory factor that may help the parasite to evade host immune responses in the skin. Given the capabilities of Sm 16.8 to induce IL-ira and suppress lymphoproliferation, this protein may also have a potential use as a therapeutic agent for inflammatory skin disorders.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"46 1","pages":"13-22"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19800429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Induction of cell death by myristylated death domain of p55 TNF receptor is not abolished by Iprcg-like point mutation in death domain. 死亡结构域iprcg样点突变不会消除p55 TNF受体肉芽化死亡结构域诱导细胞死亡的作用。

Journal of inflammation Pub Date : 1995-01-01

C H Kim, Y H Song, K Park, Y Oh, T H Lee

引用次数: 0

The internalized interleukin-1 activation complex in fibroblasts localizes to the Golgi apparatus. 内化的白介素-1激活复合体在成纤维细胞中定位于高尔基体。

Journal of inflammation Pub Date : 1995-01-01

G Praast, R Hofmeister, K Grube, W Hans, T Kühlwein, P H Krammer, W Falk

{"title":"The internalized interleukin-1 activation complex in fibroblasts localizes to the Golgi apparatus.","authors":"G Praast, R Hofmeister, K Grube, W Hans, T Kühlwein, P H Krammer, W Falk","doi":"","DOIUrl":"","url":null,"abstract":"In order to investigate binding and internalization of interleukin-1 (IL-1) by confocal laser scanning microscopy, we established a model system comprising an IL-1 receptor type I (IL-1R1) overexpressing transfectant of the murine fibrosarcoma cell line L929 (L929R1) and an N-terminal FLAG-tagged human recombinant IL-1 alpha (FLAG-IL-1 alpha). The function of the transfected receptors was shown by their IL-1-induced association with a kinase activity. The biological activity of the purified FLAG-IL-1 alpha was comparable to the unmodified molecule. L929RI cells were exposed to saturating concentrations of FLAG-IL-1 alpha. Two-color fluorescence analysis revealed increasing cell surface binding of FLAG-IL-1 alpha to the receptor over 30 min. This was followed by internalization and accumulation of the ligand/receptor complex at the Golgi apparatus. After 3 hr the receptor signal significantly decreased and patches of FLAG-epitopes reappeared on the cell surface, no longer colocalized with IL-1R1. Thus, in this model, the previously assumed nuclear accumulation of IL-1 was not detected but rather localization of the internalized IL-1/IL-1R1-complex to the Golgi apparatus was found. Direct effects of IL-1 on the nucleus or the nuclear membrane therefore are unlikely.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"46 3","pages":"125-38"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19812197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Platelet-activating factor is a mediator in tumor necrosis factor/galactosamine-induced lethality. 血小板活化因子是肿瘤坏死因子/半乳糖胺致死性的中介。

Journal of inflammation Pub Date : 1995-01-01

C Libert, W Van Molle, P Brouckaert, W Fiers

引用次数: 0

How do tumor necrosis factor receptors work? 肿瘤坏死因子受体是如何工作的?

Journal of inflammation Pub Date : 1995-01-01

F Bazzoni, B Beutler

引用次数: 0