scholarly journals Suppression of interleukin 8 production by progesterone in rabbit uterine cervix

1994 ◽  
Vol 301 (1) ◽  
pp. 183-186 ◽  
Author(s):  
A Ito ◽  
K Imada ◽  
T Sato ◽  
T Kubo ◽  
K Matsushima ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Interleukin 1 ◽  
Interleukin 8 ◽  
Cervical Ripening ◽  
Transcriptional Level ◽  
Dependent Manner ◽  
Necrosis Factor Alpha ◽  
Steady State Levels ◽  
Neutrophil Chemotactic Factor

Uterine cervical fibroblasts prepared from rabbits at 23 days of gestation were found to produce spontaneously the neutrophil chemotactic factor/interleukin 8 (IL-8). When the cells were treated with recombinant human interleukin 1 alpha and 1 beta (rhIL-1 alpha and -1 beta), both cytokines similarly enhanced the production of IL-8 in a dose-dependent manner. Recombinant tumour necrosis factor alpha also enhanced its production to a lesser extent, but interleukin 6 failed to modulate the production. Physiological concentrations of progesterone suppressed both the spontaneous and IL-1-mediated production of IL-8 in parallel with the decrease in the steady-state levels of its mRNA. These suppressive actions of progesterone were offset by co-treatment of cells with a progesterone antagonist, mifepristone (RU486). In conclusion, basal and IL-1-induced IL-8 production in rabbit uterine cervical fibroblasts is down-regulated by progesterone at the transcriptional level. These results obtained in vitro and our previous observations indicating that progesterone modulates the extra-cellular matrix breakdown via the suppression of production of matrix metalloproteinases and the augmentation of production matrix metalloproteinases and the augmentation of production of their specific inhibitors (TIMP-1) [Sato, Ito, Mori, Yamashita, Hayakawa and Nagase (1991) Biochem. J. 275, 645-650] may explain the mechanisms of the maintenance of pregnancy until parturition and the acceleration of uterine cervical ripening and dilatation at term.

scholarly journals Cells isolated from the human cortical interstitium resemble myofibroblasts and bind neutrophils in an ICAM-1--dependent manner.

1997 ◽  
Vol 8 (4) ◽  
pp. 604-615 ◽  
Author(s):  
A Clayton ◽  
R Steadman ◽  
J D Williams
Keyword(s):  
Smooth Muscle Actin ◽  
Interleukin 1 ◽  
Selection Marker ◽  
Specific Marker ◽  
Dependent Manner ◽  
Alpha Smooth Muscle Actin ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Inflammatory Infiltrates

Progressive renal disease is frequently accompanied by renal interstitial inflammation and fibrosis in which the activity of resident fibroblasts may be of central importance. Because there are relatively few fibroblasts in the normal cortical interstitium and there is no specific marker to permit their identification, these cells have proved difficult to characterize in vitro. In this study, these cells were isolated and established in culture, using CD90 as a positive selection marker. Antibodies to CD90 bound to tubular epithelial cells and fibroblasts, but not to glomerular cells in kidney sections. In culture, only fibroblasts were CD90-positive. These normal renal cortical fibroblasts (RCF) were alpha-smooth muscle actin- and vimentin-positive, but desmin-, cytokeratin-, and factor VIII-negative, identifying them as myofibroblasts. They expressed platelet-derived growth factor alpha and beta receptors; CD44; and alpha 2, beta 1, and beta 3 integrin chains: this combination of markers was also characteristic of fibroblasts in sections of normal cortex. These cells were positive for ICAM-1 but negative for VCAM-1. Similarly, proliferating or growth-arrested renal cortical fibroblasts (RCF) in culture expressed ICAM-1 but not VCAM-1. The expression of VCAM-1 was detected, however, and that of ICAM-1 was increased on fibroblasts associated with inflammatory infiltrates in sections from fibrotic kidneys, and ICAM-1 and VCAM-1 were up-regulated on RCF in culture after incubation with increasing doses of interleukin-1 beta or tumor necrosis factor alpha (maximum between 24 and 48 h). These adhesion molecules were functional, and neutrophils adhered to resting and cytokine-activated RCF. Binding was maximal between 24 and 48 h after cytokine treatment and was inhibited by anti-CD18 antibodies. ICAM-1 is the principal adhesion molecule controlling inflammatory cell infiltration of the interstitium. The study presented here suggests that cortical fibroblasts may be central to the control of this infiltration.

Augmentation of cytokine-induced nitric oxide synthesis by hydrogen peroxide

1996 ◽  
Vol 271 (1) ◽  
pp. L114-L120 ◽  
Author(s):  
S. A. Milligan ◽  
M. W. Owens ◽  
M. B. Grisham
Keyword(s):  
Nitric Oxide ◽  
Interleukin 1 ◽  
Northern Blotting ◽  
Oxidation Products ◽  
Tnf Alpha ◽  
Inos Mrna ◽  
Transcriptional Level ◽  
Necrosis Factor Alpha ◽  
Steady State Levels ◽  
Stimulation Of

The inducible isoform of nitric oxide synthase (iNOS) is induced upon stimulation of cells with cytokines and lipopolysaccharide (LPS). Stimulation of rat pleural mesothelial cells with combinations of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), and LPS induced the synthesis of nitric oxide as measured by the oxidation products nitrite (NO2-) and nitrate (NO3-). Addition of 25-50 microM H2O2 to the cytokines significantly augmented the synthesis of NO2- and NO3-. Stimulation with IL-1 beta and TNF-alpha plus H2O2 or IL-1 beta and LPS plus H2O2 increased the synthesis of NO2- and NO3- by 3.8- and 3.5-fold, respectively. These effects were inhibited by NG-nitro-L-arginine methyl ester and cycloheximide as well as by catalase. Immunoblotting demonstrated that H2O2 augmented cytokine-induced synthesis of iNOS protein. These effects were inhibited by certain antioxidants and metal chelators, suggesting that the hydroxyl radical may mediate the oxidant-induced effect. Northern blotting demonstrated that H2O2 greatly augmented steady-state levels of iNOS mRNA, suggesting that H2O2 acted in part at the transcriptional level.

scholarly journals Gold Clusters Attenuate Inflammation in Rat Mesangial Cells via Inhibiting the Activation of NF-κB Pathway

Nanomaterials ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 712
Author(s):  
Jinling Yuan ◽  
Kaixiao Hou ◽  
Yawen Yao ◽  
Zhongying Du ◽  
Cao Lu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mesangial Cells ◽  
Interleukin 1 ◽  
Kidney Injury ◽  
Gold Clusters ◽  
No Production ◽  
Dependent Manner ◽  
Necrosis Factor Alpha ◽  
Incidence And Mortality

Sepsis-induced acute kidney injury (AKI) with high incidence and mortality rates remains a great challenge in the clinic; thus, novel therapies need to be developed urgently. This complication is associated with an overwhelming systemic inflammatory response. The aim of this study was to evaluate the potential effects and possible mechanisms of gold clusters on septic AKI in vitro. Rat mesangial HBZY-1 cells were treated with peptide-templated gold clusters under lipopolysaccharide (LPS) stimulation. The LPS-induced expression of pro-inflammatory cytokines was measured, including tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6). Our data showed that the LPS-induced transcription and secretion of these cytokines were suppressed by pretreatment of gold clusters in a dose-dependent manner. Cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) also play key roles in septic AKI and both of them are induced upon LPS-stimulation in mesangial cells. Our results further showed that pretreatment with gold clusters dramatically inhibited the LPS-stimulated transcription and expression of COX2 and iNOS, and the subsequent prostaglandin E2 (PGE2) and nitric oxide (NO) production in HBZY-1 cells. Since these factors are involved in the NF-κB pathway upon LPS stimulation, the potential roles of gold clusters on the NF-κB pathway were further determined. We found that LPS-induced NF-κB activation was suppressed in gold clusters-pretreated HBZY-1 cells. These results demonstrated that gold clusters can attenuate LPS-induced inflammation in mesangial cells, probably via inhibiting the activation of the NF-κB pathway, suggesting a potential therapeutic approach for septic AKI.

scholarly journals Chyawanprash, An Ancient Indian Ayurvedic Medicinal Food, Regulates Immune Response in Zebrafish Model of Inflammation by Moderating Inflammatory Biomarkers

2021 ◽  
Vol 12 ◽  
Author(s):  
Acharya Balkrishna ◽  
Meenu Tomer ◽  
Moumita Manik ◽  
Jyotish Srivastava ◽  
Rishabh Dev ◽  
...  
Keyword(s):  
Interleukin 1 ◽  
Dependent Manner ◽  
Zebrafish Model ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Medicinal Food ◽  
Anti Inflammatory ◽  
Oxidative Effects

The time-tested Ayurvedic medicinal food, Chyawanprash, has been a part of the Indian diet since ancient times. It is an extremely concentrated mixture of extracts from medicinal herbs and processed minerals, known for its immunity boosting, rejuvenating, and anti-oxidative effects. In this study, we have evaluated the anti-inflammatory potential of Patanjali Special Chyawanprash (PSCP) using the zebrafish model of inflammation. Zebrafish were fed on PSCP-infused pellets at stipulated doses for 13 days before inducing inflammation through lipopolysaccharide (LPS) injection. The test subjects were monitored for inflammatory pathologies like behavioral fever, hyperventilation, skin hemorrhage, locomotory agility, and morphological anomaly. PSCP exerted a strong prophylactic effect on the zebrafish that efficiently protected them from inflammatory manifestations at a human equivalent dose. Expression levels of pro-inflammatory cytokines, like interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), and interleukin-1 beta (IL-1β), were also reduced in the LPS-stimulated zebrafish fed on PSCP-infused pellets. Skin hemorrhage, hyperventilation, and loss of caudal fins are characteristics of LPS-induced inflammation in zebrafish. PSCP prophylactically ameliorated skin hemorrhage, restored normal respiration, and prevented loss of caudal fin in inflamed zebrafish. Under in vitro conditions, PSCP reduced IL-6 and TNF-α secretion by THP-1 macrophages in a dose-dependent manner by targeting NF-κB signaling, as evident from the secreted embryonic alkaline phosphatase (SEAP) reporter assay. These medicinal benefits of PSCP can be attributed to its constitutional bioactive components. Taken together, these observations provide in vivo validation of the anti-inflammatory property and in vitro insight into the mode-of-action of Chyawanprash, a traditionally described medicinal food.

scholarly journals Inflammatory cytokines induce synthesis and secretion of gro protein and a neutrophil chemotactic factor but not β2-microglobulin in human synovial cells and fibroblasts

1989 ◽  
Vol 259 (2) ◽  
pp. 585-588 ◽  
Author(s):  
E E Golds ◽  
P Mason ◽  
P Nyirkos
Keyword(s):  
Interleukin 1 ◽  
Human Fibroblasts ◽  
Chemotactic Factor ◽  
Synovial Cells ◽  
Necrosis Factor Alpha ◽  
Normal Human ◽  
Neutrophil Chemotactic Factor ◽  
Factor Alpha ◽  
Beta 2 Microglobulin ◽  
Necrosis Factor

Exposure of human synovial cells and fibroblasts in monolayer culture to interleukin 1 results in prominent secretion of proteins with Mr values of 6000 and 7000. By N-terminal sequence analysis, the Mr-6000 protein is identified as the protein encoded by a recently described gro mRNA. The Mr-7000 protein is identical to a neutrophil chemotactic factor released from monocytes. Stimulation of normal human fibroblasts with tumour necrosis factor alpha also results in expression and secretion of these two proteins. In addition to these cytokine-induced proteins, we have identified beta 2-microglobulin as an Mr-8000 protein constitutively secreted by synovial cells.

scholarly journals Artemisinin Ameliorates Osteoarthritis by Inhibiting the Wnt/β-Catenin Signaling Pathway

2018 ◽  
Vol 51 (6) ◽  
pp. 2575-2590 ◽  
Author(s):  
Gang Zhong ◽  
Ruiming Liang ◽  
Jun Yao ◽  
Jia Li ◽  
Tongmeng Jiang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Cruciate Ligament ◽  
Interleukin 1 ◽  
Cartilage Degradation ◽  
Chondrocyte Apoptosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cell Viability Assay ◽  
Necrosis Factor Alpha ◽  
Anti Inflammatory

Background/Aims: Current drug therapies for osteoarthritis (OA) are not practical because of the cytotoxicity and severe side-effects associated with most of them. Artemisinin (ART), an antimalarial agent, is well known for its safety and selectivity to kill injured cells. Based on its anti-inflammatory activity and role in the inhibition of OA-associated Wnt/β-catenin signaling pathway, which is crucial in the pathogenesis of OA, we hypothesized that ART might have an effect on OA. Methods: The chondro-protective and antiarthritic effects of ART on interleukin-1-beta (IL-1β)-induced and OA patient-derived chondrocytes were investigated in vitro using cell viability assay, glycosaminoglycan secretion, immunofluorescence, quantitative reverse transcription-polymerase chain reaction, and western blotting. We also used OA model rats constructed by anterior cruciate ligament transection and medial meniscus resection (ACLT+MMx) in the joints to investigate the effects of ART on OA by gross observation, morphological staining, immunohistochemistry, and enzyme-linked immunosorbent assay. Results: ART exhibited potent anti-inflammatory effects by inhibiting the expression of proinflammatory chemokines and cytokines, including interleukin (IL)-1β, IL-6, tumor necrosis factor alpha, and matrix metallopeptidase-13. It also showed favorable chondro-protective effect as evidenced by enhanced cell proliferation and viability, increased glycosaminoglycan deposition, prevention of chondrocyte apoptosis, and degeneration of cartilage. Further, ART inhibited OA progression and cartilage degradation via the Wnt/β-catenin signaling pathway, suggesting that it might serve as a Wnt/β-catenin antagonist to reduce inflammation and prevent cartilage degradation. Conclusion: In conclusion, ART alleviates IL-1β-mediated inflammatory response and OA progression by regulating the Wnt/β-catenin signaling pathway. Thereby, it might be developed as a potential therapeutic agent for OA.

scholarly journals UBA1 and UBA2, Two Proteins That Interact with UBP1, a Multifunctional Effector of Pre-mRNA Maturation in Plants

2002 ◽  
Vol 22 (12) ◽  
pp. 4346-4357 ◽  
Author(s):  
Mark H. L. Lambermon ◽  
Yu Fu ◽  
Dominika A. Wieczorek Kirk ◽  
Marcel Dupasquier ◽  
Witold Filipowicz ◽  
...  
Keyword(s):  
Steady State ◽  
Rna Binding ◽  
Rna Recognition Motif ◽  
Dependent Manner ◽  
Binding Domains ◽  
Mrna Maturation ◽  
Associated Proteins ◽  
Steady State Levels ◽  
Transient Overexpression

ABSTRACT Nicotiana plumbaginifolia UBP1 is an hnRNP-like protein associated with the poly(A)+ RNA in the cell nucleus. Consistent with a role in pre-mRNA processing, overexpression of UBP1 in N. plumabaginifolia protoplasts enhances the splicing of suboptimal introns and increases the steady-state levels of reporter mRNAs, even intronless ones. The latter effect of UBP1 is promoter specific and appears to be due to UBP1 binding to the 3′ untranslated region (3′-UTR) and protecting the mRNA from exonucleolytic degradation (M. H. L. Lambermon, G. G. Simpson, D. A. Kirk, M. Hemmings-Mieszczak, U. Klahre, and W. Filipowicz, EMBO J. 19:1638-1649, 2000). To gain more insight into UBP1 function in pre-mRNA maturation, we characterized proteins interacting with N. plumbaginifolia UBP1 and one of its Arabidopsis thaliana counterparts, AtUBP1b, by using yeast two-hybrid screens and in vitro pull-down assays. Two proteins, UBP1-associated proteins 1a and 2a (UBA1a and UBA2a, respectively), were identified in A. thaliana. They are members of two novel families of plant-specific proteins containing RNA recognition motif-type RNA-binding domains. UBA1a and UBA2a are nuclear proteins, and their recombinant forms bind RNA with a specificity for oligouridylates in vitro. As with UBP1, transient overexpression of UBA1a in protoplasts increases the steady-state levels of reporter mRNAs in a promoter-dependent manner. Similarly, overexpression of UBA2a increases the levels of reporter mRNAs, but this effect is promoter independent. Unlike UBP1, neither UBA1a nor UBA2a stimulates pre-mRNA splicing. These and other data suggest that UBP1, UBA1a, and UBA2a may act as components of a complex recognizing U-rich sequences in plant 3′-UTRs and contributing to the stabilization of mRNAs in the nucleus.

scholarly journals Evaluation of Antioxidant and Anti-Inflammatory Activity of Anthocyanin-Rich Water-Soluble Aronia Dry Extracts

Molecules ◽  
2020 ◽  
Vol 25 (18) ◽  
pp. 4055 ◽  
Author(s):  
Mariusz Banach ◽  
Magdalena Wiloch ◽  
Katarzyna Zawada ◽  
Wojciech Cyplik ◽  
Wojciech Kujawski
Keyword(s):  
Lipid Peroxidation ◽  
Interleukin 1 ◽  
Radical Scavenging ◽  
Water Soluble ◽  
Anthocyanin Content ◽  
Necrosis Factor Alpha ◽  
Paramagnetic Resonance ◽  
Markers Of Inflammation ◽  
Radical Scavenging Properties

Aronia fruits contain many valuable components that are beneficial to human health. However, fruits are characterized by significant variations in chemical composition dependent on the growing conditions and harvesting period. Therefore, there is a need to formulate the extracts with a precisely defined content of health-promoting substances. Aronia dry extracts (ADE) were prepared from frozen pomace applying water extraction, followed by purification and spray-drying. Subsequently, the content of anthocyanins, phenolic acids, and polyphenols was determined. The high-quality chokeberry pomace enabled obtaining extracts with anthocyanin content much higher than the typical market standards. Moreover, it was found that the antioxidant capacity of aronia extracts exceeded those found in other fruit preparations. Antioxidant and free-radical scavenging properties were evaluated using a 2,2′-diphenyl-1-picrylhydrazyl using Electron Paramagnetic Resonance (EPR) spectroscopy (DPPH-EPR) test and Oxygen Radical Absorbance Capacity (ORAC) assay. The inhibition of lipid peroxidation and the level of inflammatory markers have been also investigated using lipopolysaccharide (LPS)-stimulated RAW 264 cells. It was revealed that ADE standardized to 25% of anthocyanins depresses the level of markers of inflammation and lipid peroxidation (Interleukin 1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), and malondialdehyde (MDA)) in in vitro conditions. Additionally, it was confirmed that ADE at all analyzed concentrations did not show any cytotoxic effect as demonstrated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.

scholarly journals Cytokine production by primary bone marrow megakaryocytes

Blood ◽  
1994 ◽  
Vol 84 (12) ◽  
pp. 4151-4156 ◽  
Author(s):  
S Jiang ◽  
JD Levine ◽  
Y Fu ◽  
B Deng ◽  
R London ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Interleukin 1 ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Gm Csf

Primary human bone marrow megakaryocytes were studied for their ability to express and release cytokines potentially relevant to their proliferation and/or differentiation. The purity of the bone marrow megakaryocytes was assessed by morphologic and immunocytochemical criteria. Unstimulated marrow megakaryocytes constitutively expressed genes for interleukin-1 beta (IL-1 beta), IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor-alpha (TNF-alpha), by the polymerase chain reaction (PCR) and Northern blot analysis. At the protein level, megakaryocytes secreted significant amounts of IL-1 beta (53.6 +/- 3.6 pg/mL), IL-6 (57.6 +/- 15.6 pg/mL), and GM-CSF (24 +/- 4 pg/mL) but not TNF-alpha. Exposure of human marrow megakaryocytes to IL-1 beta increased the levels of IL-6 (87.3 +/- 2.3 pg/mL) detected in the culture supernatants. Transforming growth factor- beta was also able to stimulate IL-6, IL-1 beta, and GM-CSF secretion, but was less potent than stimulation with phorbol-12-myristate-13- acetate (PMA). The secreted cytokines acted additively to maintain and increase the number of colony-forming unit-megakaryocytes colonies (approximately 35%). These studies demonstrate the production of multiple cytokines by isolated human bone marrow megakaryocytes constitutively or stimulated in vitro. The capacity of human megakaryocytes to synthesize several cytokines known to modulate hematopoietic cells supports the concept that there may be an autocrine mechanism operative in the regulation of megakaryocytopoiesis.

scholarly journals Micrococcus luteus Teichuronic Acids Activate Human and Murine Monocytic Cells in a CD14- and Toll-Like Receptor 4-Dependent Manner

2001 ◽  
Vol 69 (4) ◽  
pp. 2025-2030 ◽  
Author(s):  
Shuhua Yang ◽  
Shunji Sugawara ◽  
Toshihiko Monodane ◽  
Masahiro Nishijima ◽  
Yoshiyuki Adachi ◽  
...  
Keyword(s):  
Lipid A ◽  
Micrococcus Luteus ◽  
Dependent Manner ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Necrosis Factor Alpha ◽  
Monocytic Cells ◽  
Tnf Α

ABSTRACT Teichuronic acid (TUA), a component of the cell walls of the gram-positive organism Micrococcus luteus (formerlyMicrococcus lysodeikticus), induced inflammatory cytokines in C3H/HeN mice but not in lipopolysaccharide (LPS)-resistant C3H/HeJ mice that have a defect in the Toll-like receptor 4 (TLR4) gene, both in vivo and in vitro, similarly to LPS (T. Monodane, Y. Kawabata, S. Yang, S. Hase, and H. Takada, J. Med. Microbiol. 50:4–12, 2001). In this study, we found that purified TUA (p-TUA) induced tumor necrosis factor alpha (TNF-α) in murine monocytic J774.1 cells but not in mutant LR-9 cells expressing membrane CD14 at a lower level than the parent J774.1 cells. The TNF-α-inducing activity of p-TUA in J774.1 cells was completely inhibited by anti-mouse CD14 monoclonal antibody (MAb). p-TUA also induced interleukin-8 (IL-8) in human monocytic THP-1 cells differentiated to macrophage-like cells expressing CD14. Anti-human CD14 MAb, anti-human TLR4 MAb, and synthetic lipid A precursor IVA, an LPS antagonist, almost completely inhibited the IL-8-inducing ability of p-TUA, as well as LPS, in the differentiated THP-1 cells. Reduced p-TUA did not exhibit any activities in J774.1 or THP-1 cells. These findings strongly suggested that M. luteus TUA activates murine and human monocytic cells in a CD14- and TLR4-dependent manner, similar to LPS.

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