Journal of inflammation最新文献_第3页

Neutrophil structural changes associated with chronic endotoxemia and lung injury. 中性粒细胞结构改变与慢性内毒素血症和肺损伤相关。

Journal of inflammation Pub Date : 1998-01-01

M E Klut, S F van Eeden, J C Hogg

{"title":"Neutrophil structural changes associated with chronic endotoxemia and lung injury.","authors":"M E Klut, S F van Eeden, J C Hogg","doi":"","DOIUrl":"","url":null,"abstract":"Previous studies showed that chronic endotoxemia induces thickening of the alveolar wall of rabbits. The present study examines cellular changes associated with this process and attempts to define the role of PMN in this response. Rabbits received i.v. injections of either Escherichia coli lipopolysaccharide (LPS) or saline (control), 2-3 times weekly, for 28 weeks. Peripheral blood mature and immature polymorphonuclear leukocyte (PMN) cell counts were determined on Wright-stained blood smears. Lung histological analysis was performed by both light and electron microscopy. FITC-Maclura pomifera was used to identify type II cells and diaminobenzidine tetrahydrochloride-H2O2 was employed to localize peroxidase. The results show that the LPS-induced neutrophilia is associated with an increase in the circulating band cells which is consistent with active bone marrow release. PMN in the pulmonary microvessels display structural features characteristic of phagocytosis and active macromolecule synthesis. Endothelial cells, adjacent to these PMN, show numerous coated pits and large inclusions suggestive of endocytosis. The LPS-induced thickening of the alveolar wall is associated with leukocyte migration into the interstitial and alveolar spaces. Some interstitial PMN are fragmented and surrounded by dispersed elements of the connective tissue, while others appear activated and are closely associated with hyperactive fibroblasts and alveolar type II cells. The number of alveolar type II cells has increased twofold. These results show that chronic endotoxemia in rabbits causes structural changes in PMN, endothelium, interstitium, and epithelium. PMN structural changes are consistent with enhanced functional properties and their close association with modified regions of the lung parenchyma suggest that PMN play an important role in the process of this lung injury and repair.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"48 1","pages":"1-12"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20297693","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

Transmembrane TNF is sufficient to induce localized tissue toxicity and chronic inflammatory arthritis in transgenic mice. 跨膜TNF足以诱导转基因小鼠局部组织毒性和慢性炎性关节炎。

Journal of inflammation Pub Date : 1996-01-01

S Georgopoulos, D Plows, G Kollias

{"title":"Transmembrane TNF is sufficient to induce localized tissue toxicity and chronic inflammatory arthritis in transgenic mice.","authors":"S Georgopoulos, D Plows, G Kollias","doi":"","DOIUrl":"","url":null,"abstract":"TNF plays a pivotal role in the pathogenesis of a broad spectrum of infectious, inflammatory, and autoimmune diseases. In addition to the secreted, mature 17 kD form, TNF exists as a bioactive precursor 26 kD transmembrane protein. Transmembrane TNF signaling has been directly associated with specific immune mechanisms, including the contact-dependent lymphocyte and monocyte-mediated cell killing and the CD40 ligand-independent, T cell-mediated polyclonal B cell activation. In previous studies, we have reported that mice expressing 3'-UTR modified human TNF transgenes develop chronic inflammatory polyarthritis with a 100% phenotypic penetrance and timed disease onset. In additional experiments, we have also shown that high-level expression of human TNF in lymphoid cells of transgenic mice results in both local (thymic hypoplasia) and systemic (ischaemia, tissue necrosis, and wasting) TNF-mediated pathology. In this study we show that transgenic mice expressing a T cell-targeted membrane-associated mutant human TNF alpha protein are displaying only local TNF-mediated pathologies, ranging from lymphoid tissue derangements to proliferative synovitis and chronic inflammatory arthritis. These results demonstrate that in vivo, at least part of the pathogenic activities of TNF alpha may be assigned to the functioning of its uncleaved, membrane-associated form.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"46 2","pages":"86-97"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19708326","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

Microtubule-active agents mimic lipopolysaccharides in priming macrophages for enhanced arachidonic acid metabolism. 微管活性剂在巨噬细胞中模拟脂多糖，以增强花生四烯酸代谢。

Journal of inflammation Pub Date : 1996-01-01

N Veis, A Rosen, A Aderem

{"title":"Microtubule-active agents mimic lipopolysaccharides in priming macrophages for enhanced arachidonic acid metabolism.","authors":"N Veis, A Rosen, A Aderem","doi":"","DOIUrl":"","url":null,"abstract":"Macrophages play a crucial role in inflammation and host defense, in part, by secreting metabolites of arachidonic acid (20:4). Bacterial lipopolysaccharides (LPS) are poor agonists of the 20:4 cascade, but do have the capacity to prime macrophages for greatly increased 20:4 metabolism upon subsequent stimulation with activators of protein kinase C (PKC). The microtubule-stabilizing agent, taxol, mimics many of the effects of LPS in macrophages. We demonstrate in this study that taxol, like LPS, primes murine peritoneal macrophages for an enhanced release of 20:4 in response to both phorbol 12-myristate 13-acetate (PMA) and zymosan. Taxol and LPS, when used at maximum concentrations, acted additively to prime macrophages for PMA-stimulated release of 20:4, suggesting that the two agents signal through different pathways. Interestingly, agents that stimulate the depolymerization of microtubules, colchicine and nocodazole, also primed macrophages for an enhanced release of 20:4 in response to PMA, however, they did not prime when zymosan was the stimulus. We conclude that agents that disrupt the microtubule network prime resident peritoneal macrophages for enhanced release of 20:4.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"46 2","pages":"106-13"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19708329","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

Defective translation of tumor necrosis factor mRNA in lipopolysaccharide-tolerant macrophages. 脂多糖耐受巨噬细胞中肿瘤坏死因子mRNA翻译缺陷。

Journal of inflammation Pub Date : 1996-01-01

A Marchant, C Gueydan, L Houzet, Z Amraoui, A Sels, G Huez, M Goldman, V Kruys

{"title":"Defective translation of tumor necrosis factor mRNA in lipopolysaccharide-tolerant macrophages.","authors":"A Marchant, C Gueydan, L Houzet, Z Amraoui, A Sels, G Huez, M Goldman, V Kruys","doi":"","DOIUrl":"","url":null,"abstract":"Macrophage activation by lipopolysaccharide (LPS) results in the translational activation of tumor necrosis factor (TNF) mRNA. The initial phase of macrophage activation is followed by a refractory state called LPS tolerance characterized by an impaired TNF production in response to a secondary LPS challenge. LPS-tolerant macrophages contain high amounts of TNF mRNA, suggesting a translational regulation of TNF biosynthesis. The induction of LPS tolerance was studied in RAW 264.7 macrophages stably transfected with a chloramphenicol acetyl-transferase (CAT) reporter gene construct driven by a constitutive cytomegalovirus promoter and containing the 3' untranslated region of the murine TNF gene. We found that primary stimulation of transfected cells by LPS (1 ng/ml, 12 hr) resulted in a marked suppression (80%) of CAT accumulation in response to a secondary LPS challenge (1 microgram/ml, 6 hr). In contrast, the accumulation of CAT mRNA was not influenced by LPS tolerance. Using the same CAT reporter, we observed that the serine/threonine phosphatases 1 and 2A inhibitor okadaic acid induced TNF mRNA translation and that this activation was not inhibited by LPS-tolerance. In conclusion, these data indicate that deficient production of TNF in LPS-tolerant macrophages in response to a second LPS challenge is characterized by a defective translation of TNF mRNA. However, this hyporesponsiveness to LPS is specific, since translation of TNF mRNA induced by okadaic acid is not inhibited in LPS-tolerant macrophages.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"46 2","pages":"114-23"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19708332","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

Stimulation of the T-cell antigen receptor-CD3 complex signaling pathway by the tyrosine phosphatase inhibitor pervanadate is mediated by inhibition of CD45: evidence for two interconnected Lck/Fyn- or zap-70-dependent signaling pathways. 酪氨酸磷酸酶抑制剂过钒酸盐刺激t细胞抗原受体- cd3复合物信号通路是通过抑制CD45介导的:两个相互关联的Lck/Fyn或zap-70依赖性信号通路的证据。

Journal of inflammation Pub Date : 1996-01-01

V Imbert, D Farahifar, P Auberger, D Mary, B Rossi, J F Peyron

{"title":"Stimulation of the T-cell antigen receptor-CD3 complex signaling pathway by the tyrosine phosphatase inhibitor pervanadate is mediated by inhibition of CD45: evidence for two interconnected Lck/Fyn- or zap-70-dependent signaling pathways.","authors":"V Imbert, D Farahifar, P Auberger, D Mary, B Rossi, J F Peyron","doi":"","DOIUrl":"","url":null,"abstract":"The tyrosine phosphatase specific inhibitor pervanadate is a potent activator of T lymphocytes through induction of tyrosine phosphorylation and downstream events of the activation cascade. Using CD45- or CD3-negative variants of the Jurkat leukemic T-cell line we show that the different biochemical events induced by pervanadate appeared to be dependent on the presence at the cell surface of either CD45 or CD3. CD45-dependent events such as tyrosine phosphorylation of Shc, activation of nuclear factor-kappa B (NF-kappa B), activator protein-1 (AP-1), transcription factors, and stimulation of interleukin-2 (IL-2) promoter and of CD69 and CD25 surface expression paralleled activation of the tyrosine kinases lck and fyn. By contrast, stimulation of calcium influx, a CD3-dependent event, paralleled zap-70 activation. The data demonstrate that the T-cell antigen receptor-CD3 (TcR-CD3) complex is functionally linked to two different protein tyrosine kinase (PTK) modules with separate specific functions and that CD45 may be an important regulator of this coupling.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"46 2","pages":"65-77"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19707203","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

Bacteria and bacterial cell wall constituents induce the production of regulatory cytokines in dendritic cell clones. 细菌和细菌细胞壁成分诱导树突状细胞克隆中调节性细胞因子的产生。

Journal of inflammation Pub Date : 1996-01-01

S Riva, M L Nolli, M B Lutz, S Citterio, G Girolomoni, C Winzler, P Ricciardi-Castagnoli

{"title":"Bacteria and bacterial cell wall constituents induce the production of regulatory cytokines in dendritic cell clones.","authors":"S Riva, M L Nolli, M B Lutz, S Citterio, G Girolomoni, C Winzler, P Ricciardi-Castagnoli","doi":"","DOIUrl":"","url":null,"abstract":"The primary function of dendritic cells (DC) is the uptake, processing, and presentation of antigens to unprimed T cells, but the regulation of these functions is largely unknown. The study of the signals that maintain DC in a resting state or that drive their activation has been hampered by the difficulties in obtaining pure DC populations. The availability of immortalized DC clones from different tissues (spleen and skin) allowed us to investigate the regulation of cytokine production in response to physiological signals in the absence of contaminating cells. The DC clones exhibited the phenotypical and functional features of DC precursors and could phagocytose, albeit at a low rate, whole bacteria. Heat-inactivated bacteria and bacterial cell wall products were tested for cytokine induction. Lipopolysaccharide, lipoteichoic acid, and gram-negative bacteria were potent inducers of tumor necrosis factor alpha and interleukin 6 release, whereas gram-positive bacteria were less efficient. The results suggest that microbial infections can directly promote cytokine DC release of relevant inflammatory responses as well as in the autocrine activation of DC.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"46 2","pages":"98-105"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19708330","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 drives human monocytes to CD16 positive macrophages. 白细胞介素-10驱动人单核细胞转化为CD16阳性巨噬细胞。

Journal of inflammation Pub Date : 1996-01-01

J C Calzada-Wack, M Frankenberger, H W Ziegler-Heitbrock

引用次数: 0

Sequence, genomic organization, and chromosome localization of the mouse TRADD gene. 小鼠TRADD基因的序列、基因组组织和染色体定位。

Journal of inflammation Pub Date : 1995-01-01

M G Pan, J Xiong, N G Copeland, D J Gilbert, N A Jenkins, D V Goeddel

{"title":"Sequence, genomic organization, and chromosome localization of the mouse TRADD gene.","authors":"M G Pan, J Xiong, N G Copeland, D J Gilbert, N A Jenkins, D V Goeddel","doi":"","DOIUrl":"","url":null,"abstract":"Signals triggered by tumor necrosis factor (TNF) are mediated by its two receptors: the 55 kDa TNF receptor one (TNF-R1) and the 75 kDa TNF receptor two (TNF-R2). Activation of TNF-R1 induces cell death, NF-kappa B activation, inflammatory response and anti-viral activity, while TNF-R2 mainly stimulates cell proliferation and NF-kappa B activation. The TNF-R2-associated factor TRAF2 has been shown to mediate activation of NF-kappa B by TNF-R2 and CD40. The human TNF-R1-associated death domain protein (TRADD) induces cell death and NF-kappa B activation when overexpressed. Here we describe the cloning and gene structure of the mouse homolog of TRADD. Mouse TRADD shares 75% overall amino acid sequence identity with human TRADD, suggesting high conservation of function. Mouse TRADD specifically interacts with wild type TNF-R1 but not with a truncated mutant TNF-R1 lacking its C-terminal 20 amino acids. Like human TRADD, mouse TRADD also induces activation of NF-kappa B and cell death. The expression of TRADD in mouse embryo appears developmentally regulated. The mTRADD gene contains four exons, with the fourth exon encoding all of the death domain. The mouse TRADD gene was localized to the distal region of chromosome 8.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"46 3","pages":"168-75"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19813299","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

NF-kappa B is activated during acute inflammation in vivo in association with elevated endothelial cell adhesion molecule gene expression and leukocyte recruitment. NF-kappa B在体内急性炎症期间被激活，与内皮细胞粘附分子基因表达升高和白细胞募集有关。

Journal of inflammation Pub Date : 1995-01-01

A M Manning, F P Bell, C L Rosenbloom, J G Chosay, C A Simmons, J L Northrup, R J Shebuski, C J Dunn, D C Anderson

{"title":"NF-kappa B is activated during acute inflammation in vivo in association with elevated endothelial cell adhesion molecule gene expression and leukocyte recruitment.","authors":"A M Manning, F P Bell, C L Rosenbloom, J G Chosay, C A Simmons, J L Northrup, R J Shebuski, C J Dunn, D C Anderson","doi":"","DOIUrl":"","url":null,"abstract":"Leukocytes accumulate at sites of inflammation in response to the induced expression of endothelial cell adhesion molecules. The nuclear transcription factor kappa B (NF-kappa B) plays a critical role in the cytokine-induced expression of these genes in cultured endothelium. We examined the relationship between NF-kappa B activation and endothelial cell adhesion molecule gene expression in vivo during the initiation of acute inflammation. Nuclear NF-kappa B DNA-binding activity was rapidly increased within lung and heart tissues of rats administered endotoxin, consistent with the translocation of NF-kappa B complexes from the cytoplasm to the nucleus. This NF-kappa B was composed of p50 and p65 subunits, and could bind NF-kappa B elements in the E-selectin promoter. NF-kappa B activation was maximal within 30 min and persisted for at least 3 hr after endotoxin treatment. NF-kappa B activation preceded the transcriptional activation of the P-selectin, E-selectin, VCAM-1, and ICAM-1 genes. In the lung, increased expression of P-selectin and ICAM-1 protein was detected immunohistochemically. These molecular events were temporally associated with the sequestration of leukocytes and the development of pulmonary inflammation. NF-kappa B activation is therefore an early event in the initiation of acute inflammation in vivo. This molecular pathway may be of consequence in the pathogenesis of acute inflammatory disease.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"45 4","pages":"283-96"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19833213","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

Macrophage migration inhibitory factor: a counter-regulator of glucocorticoid action and critical mediator of septic shock. 巨噬细胞迁移抑制因子:糖皮质激素作用的反调节因子和败血性休克的关键介质。

Journal of inflammation Pub Date : 1995-01-01

T Calandra, R Bucala

{"title":"Macrophage migration inhibitory factor: a counter-regulator of glucocorticoid action and critical mediator of septic shock.","authors":"T Calandra, R Bucala","doi":"","DOIUrl":"","url":null,"abstract":"Recent studies have led to the discovery of a mediator that acts as an endogenous counter-regulator of glucocorticoid action within the immune system. Isolated as a product of anterior pituitary cells, this protein was found to have the sequence of macrophage migration inhibitory factor (MIF), one of the first cytokine activities to be described. Macrophages and T cells release MIF in response both to various inflammatory stimuli and upon incubation with low concentrations of glucocorticoids. The glucocorticoid-induced secretion of MIF is tightly regulated and decreases at high, anti-inflammatory steroid concentrations. Once secreted, MIF \"overrides\" the anti-inflammatory and immunosuppressive effects of steroids on macrophage and T-cell cytokine production. The physiological role of MIF thus appears to be to counter-balance steroid inhibition of the inflammatory response. Anti-MIF antibodies fully protect animals from experimentally induced gram-negative or gram-positive septic shock, an effect that may be the result of the increased anti-inflammatory effects of glucocorticoids after neutralization of endogenous MIF. Anti-MIF therapeutic strategies are presently under development and may prove to be a means to modulate cytokine production in septic shock as well as in other inflammatory disease states.","PeriodicalId":79405,"journal":{"name":"Journal of inflammation","volume":"47 1-2","pages":"39-51"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19877892","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