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A role for lymphocytes and cytokines on the eosinophil migration induced by LPS
Castro-Faria-Neto, Hugo C;Penido, Carmen M;Larangeira, Andréa P;Silva, Adriana R;Bozza, Patrícia T;
Memórias do Instituto Oswaldo Cruz , 1997, DOI: 10.1590/S0074-02761997000800026
Abstract: in the present work we review the existing evidence for a lps-induced cytokine-mediated eosinophil accumulation in a model of acute inflammation. intrathoracic administration of lps into rodents (mice, rats or guinea pigs) induces a significant increase in the number of eosinophils recovered from the pleural fluid 24 hr later. this phenomenon is preceded by a neutrophil influx and accompanied by lymphocyte and monocyte accumulation. the eosinophil accumulation induced by lps is not affected by inhibitors of cyclo or lipoxygenase nor by paf antagonists but can be blocked by dexamethasone or the protein synthesis inhibitor cycloheximide. transfer of cell-free pleural wash from lps injected rats (lps-pw) to naive recipient animals induces a selective eosinophil accumulation within 24 hr. the eosinophilotactic activity present on the lps-pw has a molecular weight ranging between 10 and 50 kda and its effect is abolished by trypsin digestion of the pleural wash indicating the proteic nature of this activity. the production of the eosinophilotactic activity depends on the interaction between macrophages and t-lymphocytes and its effect can not be blocked by anti-il-5 monoclonal antibodies. accumulated evidence suggest that the eosinophil accumulation induced by lps is a consequence of a eosinophilotactic cytokine produced through macrophage and t-cell interactions in the site of a lps-induced inflammatory reaction.
A role for lymphocytes and cytokines on the eosinophil migration induced by LPS
Castro-Faria-Neto Hugo C,Penido Carmen M,Larangeira Andréa P,Silva Adriana R
Memórias do Instituto Oswaldo Cruz , 1997,
Abstract: In the present work we review the existing evidence for a LPS-induced cytokine-mediated eosinophil accumulation in a model of acute inflammation. Intrathoracic administration of LPS into rodents (mice, rats or guinea pigs) induces a significant increase in the number of eosinophils recovered from the pleural fluid 24 hr later. This phenomenon is preceded by a neutrophil influx and accompanied by lymphocyte and monocyte accumulation. The eosinophil accumulation induced by LPS is not affected by inhibitors of cyclo or lipoxygenase nor by PAF antagonists but can be blocked by dexamethasone or the protein synthesis inhibitor cycloheximide. Transfer of cell-free pleural wash from LPS injected rats (LPS-PW) to naive recipient animals induces a selective eosinophil accumulation within 24 hr. The eosinophilotactic activity present on the LPS-PW has a molecular weight ranging between 10 and 50 kDa and its effect is abolished by trypsin digestion of the pleural wash indicating the proteic nature of this activity. The production of the eosinophilotactic activity depends on the interaction between macrophages and T-lymphocytes and its effect can not be blocked by anti-IL-5 monoclonal antibodies. Accumulated evidence suggest that the eosinophil accumulation induced by LPS is a consequence of a eosinophilotactic cytokine produced through macrophage and T-cell interactions in the site of a LPS-induced inflammatory reaction.
Tissue-specific cytokine release from human extra-placental membranes stimulated by lipopolysaccharide in a two-compartment tissue culture system
Natalie W Thiex, Mark C Chames, Rita K Loch-Caruso
Reproductive Biology and Endocrinology , 2009, DOI: 10.1186/1477-7827-7-117
Abstract: Gestational membranes were collected from healthy non-laboring caesarean deliveries at term. Full-thickness membranes from each placenta were cut into pieces, mounted on Transwell frames, and placed in culture wells to create a two-compartment culture with the gestational membranes serving as the barrier between compartments. The LPS (100 ng/ml) was added to the amniotic, choriodecidual or both chambers of the culture, and cytokines were assayed in the medium of the amniotic and choriodecidual chambers after 8 h of LPS exposure. Cytokine concentrations were analyzed by two-way analysis of variance for effects of treatment and side specificity of cytokine release from the membranes.LPS exposure on the choriodecidual side of the membranes significantly increased TNF-alpha, IL-6, IL-10 and IL-8 in the choriodecidual compartment, whereas TNF-alpha was the only cytokine observed to increase in the amniotic compartment. When LPS treatment was to the amniotic side of the membranes, there were significant increases in TNF-alpha and IL-6 in the amniotic compartment as well as increased concentrations of TNF-alpha, IL-6 and IL-8 in the choriodecidual compartment; however, there were no statistically significant differences for IL-10 in either compartment. No statistically significant differences were observed for IL-1beta, TGF-beta or IL-4 concentrations in response to LPS, regardless of the exposure modality.The amnion and choriodecidua exhibited distinct patterns of response to LPS with evidence of inflammatory signaling across the layers of the gestational membranes. These results suggest a complicated network of signaling within the gestational membranes, in which cytokine- and tissue-specific responses to inflammatory stimulation may have important implications for maintaining pregnancy in the challenge of microbial invasion of the uterine compartment.Although cytokines were initially described as immune cell messengers, cytokine expression occurs in non-immune cells, in
Inhibition of nitric oxide and inflammatory cytokines in LPS-stimulated murine macrophages by resveratrol, a potent proteasome inhibitor
Asaf A Qureshi, Xiu Guan, Julia C Reis, Christopher J Papasian, Sandra Jabre, David C Morrison, Nilofer Qureshi
Lipids in Health and Disease , 2012, DOI: 10.1186/1476-511x-11-76
Abstract: The present results indicate that resveratrol, pterostilbene, and morin hydrate caused significant inhibition (>70% to 90%; P?<?0.02) in the activities of chymotrypsin-like, trypsin-like, and post-acidic (post-glutamase) proteasome sites in RAW 264.7 cells at a dose of only 20 μM. These compounds also inhibited the production of NO by RAW-264.7 cells stimulated with LPS alone (>40%; P?<?0.05), or LPS?+?interferon-γ (IFN-γ; >60%; P?<?0.02). Furthermore, resveratrol, pterostilbene, morin hydrate, and quercetin suppressed secretion of TNF-α (>40%; P?<?0.05) in LPS-stimulated RAW 264.7 cells, and suppressed NF-κB activation (22% to 45%; P?<?0.05) in LPS-stimulated HEK293T cells. These compounds also significantly suppressed LPS-induced expression of TNF-α, IL-1β, IL-6, and iNOS genes in RAW 264.7 cells, and also in thioglycolate-elicited peritoneal macrophages from C57BL/6 and BALB/c mice.The present results clearly demonstrate that resveratrol and pterostilbene are particularly potent proteasome inhibitors that suppress expression of genes, and production of inflammatory products in LPS-stimulated RAW 264.7 cells, and macrophages from C57BL/6 and BALB/c mice. Resveratrol and pterostilbene which are present in grapes, blueberries, and red wine, have been implicated as contributing factors to the lower incidence of cardiovascular disease in the French population, despite their relatively high dietary fat intake. Consequently, it appears likely that the beneficial nutritional effects of resveratrol and pterostilbene are due at least in part, to their ability to inhibit NF-κB activation by the proteasome, thereby suppressing activation of pro-inflammatory cytokines and iNOS genes, resulting in decreased secretion of TNF-α, IL-1β, IL-6, and NO levels, in response to inflammatory stimuli. This is the first report demonstrating that resveratrol and pterostilbene act as proteasome inhibitors, thus providing a mechanism for their anti-inflammatory effects.Alterations in normal
IL-21 Modulates Release of Proinflammatory Cytokines in LPS-Stimulated Macrophages through Distinct Signaling Pathways  [PDF]
Su-nan Li,Wei Wang,Shou-peng Fu,Jian-fa Wang,Hong-mei Liu,Shan-shan Xie,Bing-run Liu,Yang Li,Qing-kang Lv,Zhi-qiang Li,Wen-jing Xue,Bing-xu Huang,Wei Chen,Ju-xiong Liu
Mediators of Inflammation , 2013, DOI: 10.1155/2013/548073
Abstract: The aim of this study was to investigate the anti-inflammatory effect of IL-21 on LPS-induced mouse peritoneal macrophages. The results showed that IL-21 significantly inhibited LPS-induced mRNA expression of IL-1β, TNF-α, and IL-6 in macrophages, but not of IFN-γ, IL-10, CCL5, or CXCL2. ELISA analysis showed that IL-21 also suppressed LPS-induced production of TNF-α and IL-6 in culture supernatants. Western blot analysis showed that IL-21 clearly inhibited ERK and IκBα phosphorylation and NF-κB translocation in LPS-stimulated macrophages, but it increased STAT3 phosphorylation. Flow cytometric and Western blot analysis showed that IL-21 decreased M1 macrophages surface markers expression of CD86, iNOS, and TLR4 in LPS-stimulated cells. All results suggested that IL-21 decreases IL-6 and TNF-α production via inhibiting the phosphorylation of ERK and translocation of NF-κB and promotes a shift from the M1 to M2 macrophage phenotype by decreasing the expression of CD86, iNOS, and TLR4 and by increasing STAT3 phosphorylation in LPS-stimulated cells. 1. Introduction Interleukin-21 (IL-21) is produced by activated CD4+ T-cells, natural killer T cells (NKT cells), and follicular T helper cells. The IL-21 receptor was discovered in 2000 as an orphan receptor, first denoted as NILR for novel interleukin receptor and now as IL-21R [1, 2]. IL-21 receptor expression has been detected on CD4+ T cells, CD8+ T cells, B cells, NK cells, macrophages, and dendritic cells (DCs) [1–6], suggesting that IL-21 has a broad range of functions. In addition, the IL-21 receptor is a member of a family of receptors that share the γ chain (γc). Analogous to the other γc family cytokines, IL-21 activates both Jak1 and Jak3 [1, 7, 8], and weakly activates Stat5 proteins [9]. Stat3 appears to be the most important STAT protein for IL-21 signaling. In addition, the phosphoinositol 3-kinase/Akt (PI3K/Akt) and Ras/MAP kinase (MAPK) pathways also contribute to IL-21 signaling [10]. IL-21 also clearly has an important effect on B cells, T cells, and NK T cells. For example, IL-21 can augment anti-CD40-induced human B-cell proliferation, but it inhibits proliferation to anti-IgM and IL-4 [2] and can increase the proliferation of NK T cells in response to in vitro stimulation with anti-CD3, but only when combined with either IL-2 or IL-15 [11]. Macrophages are important innate immune cells that are strategically located throughout the body tissues, where they ingest and process foreign materials, dead cells, and debris and recruit additional macrophages in response to inflammatory signals.
BBI抑制LPS诱导的肠道上皮细胞炎性因子的表达
BBI inhibits LPSinduced expression of inflammatory cytokines in intestinal epithelial cells
 [PDF]

古俊,郭乐,刘金彪,霍文哲
GU Jun
, GUO Le, LIU Jinbiao, HUO Wenzhe

- , 2017, DOI: 10.3969/j.issn.1671-9638.2017.10.001
Abstract: 目的探讨大豆来源的胰蛋白酶抑制剂(BBI)对LPS诱导的肠道上皮细胞炎性因子表达的抑制作用及其机制。方法用MTT法检测LPS和BBI对肠道上皮细胞的毒性作用。先用BBI预处理肠道上皮细胞,再用LPS刺激,采用实时荧光定量PCR检测细胞内炎性因子(TNFα、IL1β、IL8和MCP1)的表达,通过NFκBluc荧光素酶质粒和蛋白质印迹法(Western Blot)检测NFκB的活性。 结果LPS最大浓度(10 000 ng/mL)和BBI最大浓度(1 000 μg/mL)对细胞均无毒性作用。LPS处理可显著地上调肠道上皮细胞炎性因子(TNFα、IL1β、IL8和MCP1)的表达,其上调作用和LPS的浓度成正相关;LPS处理肠道上皮细胞3 h后炎性因子表达最高,随时间延长有所下降;LPS对肠道上皮细胞炎性因子的上调作用具有剂量和时间效应;BBI预处理肠道上皮细胞6 h时,BBI对LPS诱导肠道上皮细胞炎性因子表达的抑制作用最明显,且具有剂量效应。结论通过对肠道上皮细胞内NFκB的抑制,BBI能够显著地抑制LPS诱导炎症因子的表达
Gastrodin Inhibits Expression of Inducible NO Synthase, Cyclooxygenase-2 and Proinflammatory Cytokines in Cultured LPS-Stimulated Microglia via MAPK Pathways  [PDF]
Ji-Nan Dai, Yi Zong, Lian-Mei Zhong, Yue-Min Li, Wei Zhang, Li-Gong Bian, Qing-Long Ai, Yi-Dan Liu, Jun Sun, Di Lu
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0021891
Abstract: Background Microglial activation plays an important role in neurodegenerative diseases by producing several proinflammatory enzymes and proinflammatory cytokines. The phenolic glucoside gastrodin, a main constituent of a Chinese herbal medicine, has been known to display anti-inflammatory properties. The current study investigates the potential mechanisms whereby gastrodin affects the expression of potentially pro-inflammatory proteins by cultured murine microglial BV-2 cells stimulated with lipopolysaccharide (LPS). Methodology/Principal Findings BV-2 cells were pretreated with gastrodin (30, 40, and 60 μM) for 1 h and then stimulated with LPS (1 μg/ml) for another 4 h. The effects on proinflammatory enzymes, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), and proinflammatory cytokines, tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β), are analysed by double-immunofluorescence labeling and RT-PCR assay. To reveal the mechanisms of action of gastrodin we investigated the involvement of mitogen-activated protein kinases (MAPKs) cascades and their downstream transcription factors, nuclear factor-κB (NF-κB) and cyclic AMP-responsive element (CRE)-binding protein (CREB). Gastrodin significantly reduced the LPS-induced protein and mRNA expression levels of iNOS, COX-2, TNF-α, IL-1β and NF-κB. LPS (1 μg/ml, 30 min)-induced phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal protein kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) and this was inhibited by pretreatment of BV-2 cells with different concentrations of gastrodin (30, 40, and 60 μM). In addition, gastrodin blocked LPS-induced phosphorylation of inhibitor κB-α (IκB-α) (and hence the activation of NF-κB) and of CREB, respectively. Conclusion and Implications This study indicates that gastrodin significantly attenuate levels of neurotoxic proinflammatory mediators and proinflammatory cytokines by inhibition of the NF-κB signaling pathway and phosphorylation of MAPKs in LPS-stimulated microglial cells. Arising from the above, we suggest that gastrodin has a potential as an anti-inflammatory drug candidate in neurodegenerative diseases.
Cardiac Glycosides Inhibit LPS-induced Activation of Pro-inflammatory Cytokines in Whole Blood through an NF-kB-dependent Mechanism
V O Shah,J Ferguson,L A Hunsaker,L M Deck
International Journal of Applied Research in Natural Products , 2011,
Abstract: Summary: The process of hemodialysis (HD) produces a pro-inflammatory state that can lead to an increased risk for cardiovascular disease. In part, this is the result of activation of the pro-inflammatory transcription factor NF-kB in response to uremia as well as in response to HD itself, which not only involves exposure of blood leukocytes to abnormal surfaces but also potentially to any bacterial contamination associated with HD. Previously, we used lipopolysaccharide (LPS) to activate isolated peripheral blood mononuclear cells (PBMC), as a model of HD-induced stress, and demonstrated that specific natural products that are known to inhibit the activation of NF-kB exhibited a broad anti-inflammatory activity. These natural products, however, were not effective when whole blood was used. In the present study, a natural product library (TimTec NPL480) was screened, using whole blood, for the abilities of these natural products to protect against LPS-induced expression and secretion of the pro-inflammatory cytokines TNFa, IL-1b and IL-6. We report here that the cardiac glycosides strophanthidin, ouabain, proscillaridin A, digoxin, digitoxin and lanatoside C are effective natural products that limit the development of a pro-inflammatory state by preventing the activation of these pro-inflammatory signals. These active natural products also inhibited the stress-induced activation of NF-kB in a reporter assay, suggesting that inhibition of NF-kB is at least partly the mechanism by which these natural products protect whole blood leukocytes from activation by LPS. Industrial relevance: Media for hemodialysis is used millions of times annually for patients with end stage renal disease, each use representing a potential pro-inflammatory insult. It would be useful to have a drug that could be added to the media which would protect blood leukocytes from any pro-inflammatory activation that may accompany the dialysis procedure. A natural product, if demonstrated to have low toxicity, could be especially attractive as a drug candidate for this application.
Punch grafting in vitiligo
Jha Anil,Pandey S,Shukla V
Indian Journal of Dermatology, Venereology and Leprology , 1992,
Abstract: Thirty three patients of 15-35 years age having various types of stable vitilligo from 1-15 years duration were selected for punch grafting. Vitiligo lesions in all these patients were relatively refractory to systemic PUVA therapy tried for a period of 1 to 8 years. The technique of punch grafting was modified from the method described by Falabella and Behl. Complete responses was observed in 10 patients, still under follow up for 1 year and partial response in rest 23 patients who are under observation.
Experimental Investigation and Fabrication of Pneumatic Punch
A.K.GUPTA,P.BHARADWAJ,S.SAHGAL,P.M.PRADHAN
International Journal of Innovative Research in Science, Engineering and Technology , 2013,
Abstract: This paper presents the investigation, design and fabrication of blanking of thin sheet (0.1-2 mm) of different sheet material. The blank diameter is considered as 10 mm. The study helped to evaluate the influence of tool clearance, burr formation, sheet thickness, punch/die size and blanking layout on the sheet deformation. The punch load variation with tool travel and stress distribution in the sheet has been obtained. The results indicate that a reduction in the tool clearance increases the blanking load and formation of burr increasing or decreasing at different pressure. The objective of this paper is to study the behaviour of punch and formation of burr.
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