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1.
The effects of polysaccharide-based tissue adhesives on cell survival and inflammatory cell activation were determined using
in vitro mouse cell cultures. Cytotoxicity of tissue adhesives was evaluated by placing adhesives in direct contact with 3T3
fibroblast cells. Polysaccharide-based tissue adhesives composed of dextran aldehyde and star PEG amine were non-cytotoxic
to fibroblasts; in contrast, a commercial adhesive composed of 2-octyl cyanoacrylate was highly cytotoxic to fibroblasts.
The inflammatory potential of tissue adhesives was evaluated by exposing J774 macrophage cells to adhesives, and measuring
TNF-α release from macrophages. Polysaccharide-based tissue adhesives did not elicit inflammatory TNF-α release from macrophages.
These results suggest that polysaccharide-based tissue adhesives are non-cytotoxic and non-inflammatory; the results are therefore
significant in the design of in vitro cell culture systems to study biomaterials. 相似文献
2.
Polymer-based tissue adhesives composed of poly(vinyl alcohol) acetoacetate (PVOH acac) and cross-linking amines were investigated
for their effects on cell survival and inflammatory cell activation using in vitro mouse cell cultures. Cytotoxicity of tissue
adhesives was evaluated by placing adhesives in direct contact with 3T3 fibroblast cells. Tissue adhesives formulated from
PVOH acac and 3-aminopropyltrialkoxysilane (APS) were non-cytotoxic to fibroblasts; adhesives formulated from PVOH acac and
aminated poly(vinyl alcohol) (PVOH amine) were also non-cytotoxic to fibroblasts. In contrast, a commercial adhesive composed
of 2-octyl cyanoacrylate was highly cytotoxic to fibroblasts. The inflammatory potential of tissue adhesives was evaluated
by exposing J774 macrophage cells to adhesives, and measuring TNF-α release from macrophages. PVOH acac-based tissue adhesives
did not elicit inflammatory TNF-α release from macrophages. These results suggest that PVOH acac-based tissue adhesives are
non-cytotoxic and non-inflammatory. Such tissue adhesives represent a promising technology for a variety of medical applications,
including surgical wound closure and tissue engineering, and the results are also significant in the design of in vitro cell
culture systems to study biomaterials. 相似文献
3.
4.
Johanna Westra Berber Doornbos-van der Meer Peter de Boer Miek A van Leeuwen Martin H van Rijswijk Pieter C Limburg 《Arthritis research & therapy》2004,6(4):R384
In inflammatory processes, the p38 mitogen-activated protein kinase (MAPK) signal transduction route regulates production
and expression of cytokines and other inflammatory mediators. Tumor necrosis factor α (TNF-α) is a pivotal cytokine in rheumatoid
arthritis and its production in macrophages is under control of the p38 MAPK route. Inhibition of the p38 MAPK route may inhibit
production not only of TNF-α, but also of other inflammatory mediators produced by macrophages, and indirectly of inflammatory
mediators by other cells induced by TNF-α stimulation. Here we investigate the effects of RWJ 67657, a p38 MAPK inhibitor,
on mRNA expression and protein production of TNF-α and other inflammatory mediators, in monocyte-derived macrophages. A strong
inhibition of TNF-α was seen at pharmacologically relevant concentrations of RWJ 67657, but also inhibition of mRNA expression
of IL-1β, IL-8, and cyclooxygenase-2 was shown. Furthermore, it was shown that monocyte-derived macrophages have a high constitutive
production of matrix metalloproteinase 9, which is not affected by p38 MAPK inhibition. The results presented here may have
important implications for the treatment of rheumatoid arthritis. 相似文献
5.
Tumor necrosis factor-α (TNF-α) is released from blood-free perfused rat liver by the fungal metabolite ochratoxin A. Here
we have identified Kupffer cells as the sole source of OTA-mediated cytokine release. If single cell preparation of Kupffer
cells, hepatocytes, or sinusoidal endothelial cells were prepared from rat livers, only Kupffer cells released TNF-α upon
incubation with 2.5 μmol/l OTA. OTA failed to induce TNF-α release in the blood-free perfused isolated rat liver when Kupffer
cells were blockedin vitro by 15 μmol/l gadolinium chloride. When rats were pretreatedin vivo with the Kupffer cell depleting clodronate liposomes, OTA-mediated TNF-α release was abrogated in the isolated perfused liver
model. 相似文献
6.
Peroxisome proliferator-activated receptor gamma (PPARγ) activation by its ligands reportedly inhibits monocyte function.
However, because the concentrations of PPARγ ligands used in previous studies were higher than typically expected to activate
PPARγ, we clarified whether PPARγ ligands influence monocyte function and cell viability of the human monocyte cell line THP-1.
We determined tumor necrosis factor-alpha (TNF-α) release as a monocyte function and cell viability using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium
bromide. Both troglitazone and 15-deoxy-Δ12,14-prostaglandin J2 (15-d-PGJ2) seemed to inhibit phorbol ester-induced TNF-α release from THP-1 cells. On the other hand, neither pioglitazone
nor rosiglitazone inhibited phorbol ester-induced TNF-α release. Because the cytotoxicity of troglitazone and 15-d-PGJ2 was
significantly (p<0.05, Tukey–Kramer) stronger than that of pioglitazone and rosiglitazone, the inhibition of TNF-α release seemed to parallel
the lack of cell viability. We concluded that PPARγ ligands did not directly inhibit TNF-α release in THP-1 cells.
This revised version was published online in July 2006 with corrections to the Cover Date. 相似文献
7.
Dehydroepiandrosterone and melatonin prevent Bacillus anthracis lethal toxin-induced TNF production in macrophages 总被引:4,自引:0,他引:4
The lethal toxin of Bacillus anthracis, which is composed of two separate proteinaceous exotoxins, namely protective antigen and lethal factor, is central to the
pathogenesis of anthrax. Low levels of this toxin are known to induce release of cytokines such as tumor necrosis factor α
(TNF-α). In the present study we investigated the effect of dehydroepiandrosterone (DHEA), melatonin (MLT), or DHEA + MLT
on production of lethal toxin-induced TNF-α in mouse peritoneal macrophages. We found that treatment with DHEA significantly
inhibited the TNF-α production caused by anthrax lethal toxin. Exposure of MLT to anthrax lethal toxin-treated macrophages
also decreased the release of TNF-α to the extracellular medium as compared to the control. However, combined use of DHEA
and MLT also inhibited TNF-α release, but not more than single therapies. These results suggest that DHEA and MLT may have
a therapeutic role in reducing the increased cytokine production induced by anthrax lethal toxin.
This revised version was published online in July 2006 with corrections to the Cover Date. 相似文献
8.
Sergei Vyalov Alexis Desmoulière Giulio Gabbiani 《Virchows Archiv. B, Cell pathology including molecular pathology》1993,63(1):231-239
We have studied the formation of granulation tissue around osmotic minipumps delivering granulocyte macrophage-colony stimulating
factor (GM-CSF) chronologically in the rat using electron microscopy and immunohistochemistry at the light and electron microscopic
levels, with specific antibodies against α-smooth muscle (SM) actin and rat macrophages. At 2 and 3 days after pump implantation,
GM-CSF application produced an extensive inflammatory reaction characterized by edema and the accumulation of polymorphonuclear
cells and macrophages. Gradually, polymorphonuclear cells decreased in number and macrophages became arranged in large clusters.
The expression of α-SM actin in fibroblastic cells of the granulation tissue started from the 4th day after pump implantation
and progressed up to the 7th day. Double immunofluorescence staining showed macrophage clusters in relation to α-SM actinrich
fibroblastic cells. Electron microscopic examination confirmed that the fibroblasts containing α-SM actinpositive stress fibers
were found initially in close proximity to clustered macrophages. The delivery of plateletderived growth factor (PDGF) and
tumor necrosis factor-α (TNF-α) by the osmotic minipump induced an accumulation of macrophages, but in a much smaller number
compared with those seen after GM-CSF application; these macrophages were never assembled in clusters and, furthermore, TNF-α
and PDGF did not stimulate α-SM actin expression in fibroblastic cells. Our results suggest that after GM-CSF administration,
the cluster-like accumulation of macrophages plays an important role in stimulating α-SM actin expression in myofibroblasts.
Our results may be relevant to the understanding of the processes leading to granulation tissue formation in this and other
experimental models. 相似文献
9.
Zhengming Zhou Tao Tao Yuhong Ji Huiguang Yang Youhua Wang Chun Cheng Aiguo Shen Xiang Lu 《Cellular and molecular neurobiology》2010,30(5):701-707
Tumor necrosis factor-alpha (TNF-α) derived from activated Schwann cells (SCs) plays a critical role as an inflammatory mediator
in the peripheral nervous system disease. TNF-α could act as an autocrine mediator in SC activation. In this study, we found
knockdown Src-suppressed protein kinase C substrate (SSeCKS) expression suppressed TNF-α production induced by TNF-α, overexpression
of SSeCKS could promoted TNF-α autocrine in SCs. Such effects might be resulted in SSeCKS promoted p38 and JNK activation
in SCs treated by TNF-α. Thus present data show that while SCs activation, SSeCKS may plays an important role in the release
of inflammatory mediators. 相似文献
10.
Mast cell (MC) activation in the rheumatoid lesion provides numerous mediators that contribute to inflammatory and degradative processes, especially at sites of cartilage erosion. MC activation in rheumatoid synovial tissue has often been associated with tumour necrosis factor (TNF)-α and interleukin (IL)-1β production by adjacent cell types. By contrast, our in situ and in vitro studies have shown that the production of IL-15 was independent of MC activation, and was not related to TNF-α and IL-1β expression. Primary cultures of dissociated rheumatoid synovial cells produced all three proinflammatory cytokines, with production of IL-1β exceeding that of TNF-α, which in turn exceeded that of IL-15. In vitro cultures of synovial macrophages, synovial fibroblasts and articular chondrocytes all produced detectable amounts of free IL-15, macrophages being the most effective. 相似文献
11.
Yeo Dae Yoon Eun Sook Lee Jong Pil Park Mee Ree Kim Jun Won Lee Tae Hoon Kim Min Kyun Na Jin Hee Kim 《Biotechnology and Bioprocess Engineering》2011,16(6):1099-1105
Hizikia fusiforme is a commonly used food that possesses potent anti-bacterial, anti-fungal, and anti-inflammatory activities. The immunostimulatory
activities of aqueous extract of Hizikia fusiforme (HFAE) in RAW 264.7 macrophages and whole spleen cells were investigated. HFAE activated RAW 264.7 macrophages to produce
cytokines such as nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in
a dose-dependent manner. In addition, HFAE induced the mRNA expression of TNF-α, IL-1β, and IL-6 in RAW 264.7 macrophages.
Moreover, HFAE stimulated proliferation of whole spleen cells and reference mitogen. Taken together, the results demonstrate
that HFAE potently activates the immune function by regulating NO, TNF-α, IL-1β, and IL-6 in RAW 264.7 macrophage and promoting
spleen cell proliferation. 相似文献
12.
In the peripheral nervous system (PNS), tumor necrosis factor-alpha (TNF-α) derived from activated Schwann cells (SCs) play
a critical role as a pleiotropic mediator. In this study, we examined the function of TNF-α as an inflammatory mediator in
SCs activation. TNF-α exhibits its biological effect through two distinct surface receptors, TNF receptor 1 (TNFR1) and TNFR2.
We show here that cultured SCs express both TNFR1 and TNFR2, and that activation of these receptors by TNF-α promotes expression
of TNF-α. Meanwhile, TNF-α also increased the production of other inflammatory mediators. Furthermore, TNF-α is involved in
the induction of apoptosis through binding to TNFR in SCs. The activation of SCs by lipopolysaccharide (LPS) is partially
mediated by SCs-derived TNF-α. These findings suggest the existence of a positive feedback loop in the activation of SC via
TNF-α. This loop may be involved in the prolonged activation of SCs. Acute or chronic stimulation of TNF-α by SC at sites
of PNS inflammation may be critical in determining whether TNF-α has activational, inflammatory, or cytotoxic effects on these
cells.
Yongwei Qin and Chun Cheng contributed equally to this work. 相似文献
13.
14.
Alagappan VK McKay S Widyastuti A Garrelds IM Bogers AJ Hoogsteden HC Hirst SJ Sharma HS 《Cell biochemistry and biophysics》2005,43(1):119-129
Airflow obstruction in chronic airway disease is associated with airway and pulmonary vascular remodeling, of which the molecular
mechanisms are poorly understood. Paracrine actions of angiogenic factors released by resident or infiltrating inflammatory
cells following activation by proinflammatory cytokines in diseased airways could play a major role in the airway vascular
remodeling process. Here, the proinflammatory cytokines interleukin (IL)-1β, and tumor necrosis factor (TNF)-α were investigated
on cell cultures of human airway smooth muscle (ASM) for their effects on mRNA induction and protein release of the angiogenic
peptide, vascular endothelial growth factor (VEGF). IL-1β (0.5 ng/mL) and TNF-α (10ng/mL) each increased VEGF mRNA (3.9 and
1.7 kb) expression in human ASM cells, reaching maximal levels between 16 and 24 and 4 and 8h, respectively. Both cytokines
also induced a time-dependent release of VEGF, which was not associated with increased ASM growth. Preincubation of cells
with 1μM dexamethasone abolished enhanced release of VEGF by TNF-α. The data suggest that human ASM cells express and secrete
VEGF in response to proinflammatory cytokines and may participate in paracrine inflammatory mechanisms of vascular remodeling
in chronic airway disease. 相似文献
15.
16.
Rossol M Kaltenhäuser S Scholz R Häntzschel H Hauschildt S Wagner U 《Arthritis research & therapy》2005,7(6):R1189-R1199
Stimulation of monocytes/macrophages after cell contact with preactivated T cells has been suggested to contribute to the
excessive TNF-α production in rheumatoid arthritis (RA). In this study, T cell-contact-dependent TNF-α production by peripheral-blood
monocytes in vitro was investigated and found to be significantly lower in treated and untreated patients with RA than in healthy controls.
This suppression was not due to a general deficiency of monocytes to respond, because responses to lipopolysaccharide were
comparable in patients and controls. In agreement with the pivotal role of TNF-α in RA, T cell-dependent induction of TNF-α
in synovial macrophages was fivefold to tenfold higher than in peripheral-blood monocytes from either patients or controls.
The decreased response of peripheral-blood monocytes from patients with RA was found to be mediated by inhibitory serum factors,
because the addition of patient sera to monocytes from healthy controls suppressed TNF-α response in the co-culture assay.
Preincubation of monocytes from healthy controls with RA serum was sufficient to suppress the subsequent TNF-α response in
T cell co-cultures, indicating that inhibitory factors do indeed bind to monocyte surfaces, which might represent a regulatory
counter-action of the immune system to the long-standing and consuming autoimmune process in RA. There are some indications
that apolipoprotein A-1 might be part of this regulatory system. 相似文献
17.
Jurisic V Srdic-Rajic T Konjevic G Bogdanovic G Colic M 《The Journal of membrane biology》2011,239(3):115-122
TNF-α can induce cell death (apoptosis and necrosis), and these effects mostly depend on expression of TNF-receptor superfamily
molecules. As determination of certain intracellular enzymes like LDH, released from cultured tumor cells, reflects early
membrane alterations, we compared LDH release with changes in cell surface membrane molecule expression during culture of
K-562 cells in the presence of TNF-α. TNF-α-mediated CD45 and CD30 shedding is shown to be to be time- and dose-dependent
and associated with significant increase in LDH release, with maximal effects after 24 h of treatment. The percentage of decrease
of all examined cell surface molecules on K-562 cells after TNF-α treatment was not uniform and appeared to depend on the
respective constitutive level of expression and molecule type. The presence of these molecules was confirmed in supernatants
using Western blot analyses. These results indicated the complexity of events on the cell membrane, including early LDH release
that is associated with a difference in shedding of CD30 and CD45. Shedding of CD30 occurs before apoptosis induction, while
shedding of CD45 is associated with apoptosis. 相似文献
18.
Berg K Chatterjee A Yasmin T Shara M Bagchi D 《Molecular and cellular biochemistry》2007,300(1-2):171-175
Helicobacter pylori, in recent years, has been recognized as the major causative agent in chronic gastritis and peptic ulcer disease in humans.
H. pylori is a ubiquitous organism, with at least half of the world’s population infected. Of those individuals with peptic ulcer disease,
it is estimated that 90% of cases are caused by H. pylori. Currently, the efficacy of therapies is starting to decline due to increasing resistance rates, especially towards clarithromycin.
Due to this, new therapies are needed to combat this bacterium. It is hypothesized that cytokine release (especially interleukin-1β,
-6, -8, and TNF-α) due to H. pylori infection and the subsequent influx of inflammatory cells causes a massive release of reactive oxygen species (ROS) during
the inflammatory reaction. The ROS then cause the pathologic changes seen in the infected tissues. In this study, human gastric
adenocarcinoma cell line ATCC 1739 (a cell line not previously evaluated) was examined for its production of interleukin-1β,
-6, -8, and TNF-α when cocultured in a ratio of 10:1 H. pylori to adenocarcinoma cells, to determine its value as a model to demonstrate the inflammatory response. Results from this study
indicated that ATCC 1739 cells only reliably produced IL-8 when cocultured with H. pylori and stimulated with TNF-α. The production of IL-1β, IL-6, and TNF-α by the ATCC 1739 cells was no different in H. pylori-exposed cells than non-exposed cells. It was concluded that the ATCC 1739 cell line is not suitable to study the effects of
coculture with H. pylori on cytokine production. 相似文献
19.
Gypenoside XLIX isolated from Gynostemma pentaphyllum inhibits nuclear factor-kappaB activation via a PPAR-alpha-dependent pathway 总被引:2,自引:0,他引:2
Huang TH Li Y Razmovski-Naumovski V Tran VH Li GQ Duke CC Roufogalis BD 《Journal of biomedical science》2006,13(4):535-548
Summary Nuclear factor (NF)-κB is important in the generation of inflammation. Besides regulating lipid metabolism, peroxisome proliferator-activated receptor (PPAR)-α activators also reduce NF-κB activation to terminate activation of inflammatory pathways. Gynostemma pentaphyllum (GP) has been used to treat various inflammatory diseases and hyperlipidemia. Here, we demonstrate that GP extract and one of its main components, Gypenoside XLIX (Gyp-XLIX) inhibited LPS-induced NF-κB activation in murine macrophages. Furthermore, Gyp-XLIX restored the LPS- and TNF-α-induced decrease in cytosolic I-κBα protein expression and inhibited the translocation of NF-κB(p65) to the nucleus in THP-1 monocyte and HUVEC cells. The inhibition of LPS- and TNF-α-induced NF-κB luciferase activity in macrophages was abolished by MK-886, a selective PPAR-α antagonist. GP extract and Gyp-XLIX (EC50: 10.1 μM) enhanced PPAR-α luciferase activity in HEK293 cells transfected with the tK-PPREx3-Luc reporter plasmid and expression vectors for PPAR-α. Additionally, Gyp-XLIX specifically enhanced PPAR-α mRNA and protein expression in THP-1-derived macrophage cells. The selectivity of Gyp-XLIX for PPAR-α was demonstrated by the activation of only PPAR-α in HEK293 cells transfected with expression vectors for PPAR-α, PPAR-β/δ or PPAR-γ1 plasmids and in THP-1-derived macrophage naturally expressing all three PPAR isoforms. The present study demonstrates that Gyp-XLIX, a naturally occurring gynosaponin, inhibits NF-κB activation via a PPAR-α-dependent pathway.Tom Hsun-Wei Huang and Yuhao Li contributed equally. 相似文献