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Proinflammatory Cytokine Production (proinflammatory + cytokine_production)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Phagocytosis of Apoptotic Trophoblast Cells by Human Endometrial Endothelial Cells Induces Proinflammatory Cytokine Production

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 1 2010
Bing Peng
Citation Peng B, Koga K, Cardenas I, Aldo P, Mor G. Phagocytosis of apoptotic trophoblast cells by human endometrial endothelial cells induces proinflammatory cytokine production. Am J Reprod Immunol 2010; 64: 12,19 Problem, Apoptosis is a normal constituent of trophoblast turnover in the placenta; however in some cases, this process is related to pregnancy complications such as preeclampsia. Recognition and engulfment of these apoptotic trophoblast cells is important for clearance of dying cells. The aim of this study was to show the cross talk between human endometrial endothelial cells (HEECs) and apoptotic trophoblast cells in an in vitro coculture model and its effect on cytokine production by HEECs. Method of study, Fluorescent-labeled HEECs were cocultured with fluorescent-labeled apoptotic human trophoblast cells. Confocal microscopy and flowcytometry were used to show the interaction between these two types of cells. Cytokine profiles were determined using multiplex analysis. Results, HEECs are capable to phagocytose apoptotic trophoblasts. This activity is inhibited by the phagocytosis inhibitor cytochalasin B. Phagocytosis of apoptotic trophoblast cells induced the secretion of the proinflammatory cytokines interleukin-6 and monocyte chemoattractant protein-1 by HEECs. Conclusion, This study provides the first evidence that HEECs have an ability to phagocytose apoptotic trophoblasts. Furthermore, we demonstrated an inflammatory response of HEECs after phagocytosing the apoptotic trophoblast cells. This event may contribute to the inflammatory response in both normal pregnancy and pathologic pregnancy such as preeclampsia. [source]

Release of (1,3)-,-D-Glucan from Depth-type Membrane Filters and Their In Vitro Effects on Proinflammatory Cytokine Production

ARTIFICIAL ORGANS, Issue 8 2003
Atsushi Ohata
Abstract:, To clarify the origin of (1,3)-,-D-glucan in blood products and assess the biological activity of filter extracts, we evaluated (1,3)-,-D-glucan extraction from depth filters used to process blood products and their in vitro effects on proinflammatory cytokine production from macrophages. Cellulose or nylon filters were analyzed for (1,3)-,-D-glucan using the Fungitec G test. To evaluate the biological activity of the filter extracts, Mono Mac 6 cells (a human macrophage cell line) were cultured with filter extracts with or without lipopolysaccharide, and tumor necrosis factor-alpha (TNF-,) and interleukin-1 beta (IL-1,) concentrations in the culture media were measured. (1,3)-,-D-Glucan was released from seven cellulose filters but the nylon filter level was undetectable. Proinflammatory cytokine production ranged from 74.3% to 119.0% of the control for TNF-, and 81.2% to 115.9% for IL-1,. TNF-, and IL-1, levels were low without lipopolysaccharide. The data indicate that (1,3)-,-D-glucan in blood products is contaminated with the depth filters and that these filter extracts modulate proinflammatory cytokine production from macrophages. [source]

Sex difference in the liver of hepatocyte-specific Pten-deficient mice: A model of nonalcoholic steatohepatitis

HEPATOLOGY RESEARCH, Issue 6 2009
Yumiko Anezaki
Aim:, Nonalcoholic fatty liver disease (NAFLD) is considered to be a public health problem worldwide. NAFLD is more prevalent in men than in women. Tamoxifen, a potent estrogen receptor antagonist, causes nonalcoholic steatohepatitis (NASH), a severe form of NAFLD. Thus, there may be a sex difference that is dependent on estrogens in NAFLD and NASH. Hepatocyte-specific Pten-deficient mice exhibit hepatic lesions analogous to NASH and are considered to be a clinical model of NASH. We aimed to shed light on any sex differences in the hepatic lesions of Pten-deficient mice and the underlying mechanisms. Methods:, At 40 weeks, livers from male and female Pten-deficient mice were processed for measuring lipid content, genes expression analysis, and histological examination. Level of serum reactive oxygen species (ROS) was also determined. Seventy-six-week-old mice were used in tumor burden experiments. Results:, Hepatic steatosis, inflammation, and even carcinogenesis in Pten-deficient mice were attenuated in females compared to males. Attenuated fatty liver in females was ascribed to inactivation of sterol regulatory element binding protein-1c. Hepatic inflammation in females was suppressed via decreased ROS with increased antioxidant gene expression and decreased proinflammatory cytokine production. Anti-cancer effect in female mice was, at least in part, due to the significantly lower ratio of oleic to stearic acid in the liver. Conclusions:, Hepatic lesions in Pten-deficient mice were attenuated in females compared to males, as were human NAFLD and NASH. Some of the underlying mechanisms in sex difference appeared to be due to the change of gene expression, dependent on estrogens. [source]

Mucosal NOD2 expression and NF-,B activation in pediatric Crohn's disease

INFLAMMATORY BOWEL DISEASES, Issue 3 2008
Laura Stronati PhD
Abstract Background: Recent advances in the pathogenesis of Crohn's disease (CD) have suggested that an aberrant innate immune response initiates the cascade of events leading to T-cell activation and to disease development. NOD2 protein, which is mainly expressed by innate immunity cells, appears to play a key role against bacteria by triggering a host defense response through the activation of the transcriptor factor NF-,B and a consequent proinflammatory cytokine production. The present study was aimed at investigating the expression and activity of NOD2, NF-,B, and of 2 proinflammatory cytokines, TNF, and IL-1,, in mucosal biopsies of CD affected children compared to healthy controls. Methods: In all, 22 children with active CD and 10 matched controls were entered in the study. mRNA and protein expressions were detected using reverse-transcriptase polymerase chain reaction (RT-PCR) and Western blot; NF-,B binding activity was assessed by electromobility gel shift assay (EMSA). Results: NOD2 and IL-1, mRNAs were upregulated in CD children. Protein levels of NOD2, TNF,, and nuclear NF-,B, as well as the binding activity of NF-,B to a consensus DNA sequence, were significantly increased in inflamed mucosa of patients as compared to controls. Moreover, NF-,B activity was strongly upregulated in patients also when bound to the NOD2 promoter site. No difference was seen between patients and controls when NF-,B binding activity was determined in the uninflamed tissue. Conclusions: This study suggests that altered mechanisms regulating NOD2 induction, NF-,B activation and cytokine production may contribute to dysregulate the innate immune response underlying pediatric CD. (Inflamm Bowel Dis 2007) [source]

Phagocytosis of Apoptotic Trophoblast Cells by Human Endometrial Endothelial Cells Induces Proinflammatory Cytokine Production

Resident macrophages initiating and driving inflammation in a monosodium urate monohydrate crystal,induced murine peritoneal model of acute gout

ARTHRITIS & RHEUMATISM, Issue 1 2009
William John Martin
Objective To determine whether infiltrating monocytes, neutrophils, or resident macrophages contribute to the early inflammatory response to monosodium urate monohydrate (MSU) crystals in vivo. Methods MSU crystal,induced inflammation was monitored using a peritoneal model of acute gout. The production of proinflammatory cytokines (interleukin-1, [IL-1,], tumor necrosis factor , [TNF,], IL-6) by resident macrophages, infiltrating monocytes, and neutrophils during the onset of gout was determined by flow cytometry. Infiltrating and resident peritoneal cells were cultured with MSU crystals ex vivo, and proinflammatory cytokine production was determined by multiplex cytokine array. Activated macrophages on the visceral epithelial lining of the peritoneum were identified by immunofluorescence histochemistry. The inflammatory immune response to MSU crystals was then compared with the inflammatory response in mice depleted of resident macrophages by pretreatment with clodronate liposomes. Results The production of cytokines in vivo preceded the influx of Gr-1intermediate7/4+ monocytes. Monocytes and neutrophils recruited during the inflammatory phase of the response to MSU crystals failed to produce proinflammatory cytokines either in vivo, or ex vivo following restimulation with MSU crystals. Stimulation of the naive peritoneal resident cell population with MSU crystals ex vivo resulted in positive staining of resident macrophages for the proinflammatory cytokines IL-1,, TNF,, and IL-6. Depletion of the resident macrophage population resulted in a significant decrease in both MSU crystal,induced neutrophil infiltration and proinflammatory cytokine production in vivo despite the presence of infiltrating monocytes. Conclusion These data indicate that resident macrophages, rather than infiltrating monocytes or neutrophils, are important for initiating and driving the early proinflammatory phase of acute gout. [source]

TNF Alpha,308 Genotype and Renin,Angiotensin System in Hemodialysis Patients: An Effect on Inflammatory Cytokine Levels?

ARTIFICIAL ORGANS, Issue 2 2005
Gultekin Genctoy
Abstract:, Background: Renin,angiotensin system (RAS) was suggested to modulate inflammatory cytokine production. Angiotensin II was consistently shown to increase production of tumor necrosis factor alpha (TNF-,). However, inflammatory cytokines and RAS were modulated by genetic polymorphisms such as TNF-,,308 G > A and angiotensin-converting enzyme (ACE) I/D gene polymorphisms. The aim of this study was to investigate the effects of ACE and TNF-, genotypes on inflammatory cytokines in hemodialysis (HD) patients. Methods: ACE I/D and TNF-,,308 G > A genotypes, pre- and postdialysis plasma renin activity (PRA), serum ACE, interleukin-1 beta (IL-1,), and TNF-, levels were determined in 22 HD patients. Results: Predialysis serum ACE activity is correlated with TNF-, (r = 0.63; P = 0.01), and PRA was correlated with IL-1, levels (r = 0.49; P = 0.02). Pre/postdialysis IL-1, and TNF-, were similar in DD and II/ID ACE genotypes. Predialysis TNF-, and IL-1, (32.4 ± 5; 35.1 ± 4.2 vs. 28.1 ± 3.7; 26.5 ± 6.2 pg/mL; P < 0.05) and postdialysis TNF-, levels (30.4 ± 1.4 vs. 28.4 ± 0.82 pg/mL; P < 0.05) were significantly higher in TNF1/2 than TNF1/1 patients. Conclusion: ACE and TNF-,,308 G > A (1/2) gene polymorphisms may contribute to modulation of proinflammatory cytokine production and hence chronic inflammation in HD patients. [source]

Release of (1,3)-,-D-Glucan from Depth-type Membrane Filters and Their In Vitro Effects on Proinflammatory Cytokine Production

Cyclical ischaemic preconditioning modulates the adaptive immune response in human limb ischaemia,reperfusion injury

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 4 2009
P. J. Sullivan
Background: Reperfusion injury (RI) has significant local and systemic consequences. Ischaemic preconditioning (IPC) modulates RI and the innate immune response. This study examined whether IPC attenuates RI-mediated changes in lymphocyte populations and function following elective surgery. Methods: Twenty-five patients sustaining 1 h of tourniquet ischaemia during cruciate ligament reconstruction were randomized before surgery to three 5-min ischaemia cycles separated by 5 min of reperfusion, or to a control group. Systemic levels of interleukin (IL) 4 and interferon (IFN) ,, and surface expression of CD45ro/ra, CD62L and CD95 were measured. T cells were examined systemically and in stimulated serum co-culture to determine CD4/CD8 and Th1/Th2 shifts through intracellular cytokine production. Results: CD4 CD45ro cell numbers increased after RI without IPC, whereas CD8 cells expressing CD45ro and CD95 increased with IPC. Preconditioned serum in co-culture attenuated increases in CD4 and decreases in CD8 numbers, a process prevented by inhibition of antigen activation. Following RI, systemic IL-2 levels were significantly lower after IPC, whereas co-culture with post-RI serum increased proinflammatory intracellular cytokine production. Conclusion: IPC modulated T cell responses in limb RI through reduced activation and proinflammatory cytokine production by CD4 cells, while preventing CD4/CD8 derangement. IPC prevented lymphocyte-directed immune dysfunction. Copyright © 2009 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source]

The effect of deproteinized bovine bone on osteoblast growth factors and proinflammatory cytokine production

CLINICAL ORAL IMPLANTS RESEARCH, Issue 6 2010
Paolo Amerio
Abstract Objective: To test the ability of Bio-Oss® in inducing growth factors and proinflammatory cytokines that may have a role in inflammation after grafting, bone resorption, remodeling and in the homeostasis of osteoblasts. Material and methods: Normal human osteoblasts were seeded in Petri dishes containing granules of Bio-Oss®, cells were harvested after confluency and RNA was extracted. Reverse transcriptase polymerase chain reaction was performed using specific primers for osteonectin, bone sialoprotein (BSP), bone morphogenetic protein (BMP)-2 and BMP-7, platelet-derived growth factor (PDGF), interleukin 6 (IL-6), tumor necrosis factor , (TNF-,) and integrin ,1. Glycerol-3-phosphate dehydrogenase was used as the housekeeping gene and normal human osteoblasts grown on Petri dishes without Bio-Oss® granules were used as negative controls. Results: Osteoblast grown on Bio-Oss® showed a normal RNA expression of osteonectin, integrin ,1 and PDGF. However, compared with control osteoblasts it showed a reduced expression of BSP, BMP-2 and BMP-7, IL-6 and TNF-,. Conclusions: Our findings further support the evidence that Bio-Oss® is an excellent biomaterial that does not enhance the production of proinflammatory cytokines. To cite this article: Amerio P, Vianale G, Reale M, Muraro R, Tulli A, Piattelli A. The effect of deproteinized bovine bone on osteoblast growth factors and proinflammatory cytokine production. Clin. Oral Impl. Res. 21, 2010; 650,655. doi: 10.1111/j.1600-0501.2009.01881.x [source]