scholarly journals Leptomeningeal Cells Transduce Peripheral Macrophages Inflammatory Signal to Microglia in Reponse toPorphyromonas gingivalisLPS

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Yicong Liu ◽  
Zhou Wu ◽  
Xinwen Zhang ◽  
Junjun Ni ◽  
Weixian Yu ◽  
...  
Keyword(s):  
Conditioned Medium ◽  
Chronic Periodontitis ◽  
Human Monocyte ◽  
Inhibitory Effect ◽  
Mrna Levels ◽  
Proinflammatory Mediators ◽  
Raw264.7 Macrophages ◽  
Inflammatory Signals ◽  
The Mean

We report here that the leptomeningeal cells transduce inflammatory signals from peripheral macrophages to brain-resident microglia in response toPorphyromonas gingivalis (P.g.)LPS. The expression of Toll-like receptor 2 (TLR2), TLR4, TNF-α, and inducible NO synthase was mainly detected in the gingival macrophages of chronic periodontitis patients. Inin vitrostudies,P.g.LPS induced the secretion of TNF-αand IL-1βfrom THP-1 human monocyte-like cell line and RAW264.7 mouse macrophages. Surprisingly, the mean mRNA levels of TNF-αand IL-1βin leptomeningeal cells after treatment with the conditioned medium fromP.g.LPS-stimulated RAW264.7 macrophages were significantly higher than those after treatment withP.g.LPS alone. Furthermore, the mean mRNA levels of TNF-αand IL-1βin microglia after treatment with the conditioned medium fromP.g.LPS-stimulated leptomeningeal cells were significantly higher than those afterP.g.LPS alone. These observations suggest that leptomeninges serve as an important route for transducing inflammatory signals from macrophages to microglia by secretion of proinflammatory mediators during chronic periodontitis. Moreover, propolis significantly reduced theP.g.LPS-induced TNF-αand IL-1βproduction by leptomeningeal cells through inhibiting the nuclear factor-κB signaling pathway. Together with the inhibitory effect on microglial activation, propolis may be beneficial in preventing neuroinflammation during chronic periodontitis.

Molecular characterization of prophenoloxidase-1 (PPO1) and the inhibitory effect of kojic acid on phenoloxidase (PO) activity and on the development ofZeugodacus tau(Walker) (Diptera: Tephritidae)

2018 ◽  
Vol 109 (2) ◽  
pp. 236-247 ◽  
Author(s):  
H.-H. Zhang ◽  
M.-J. Luo ◽  
Q.-W. Zhang ◽  
P.-M. Cai ◽  
A. Idrees ◽  
...  
Keyword(s):  
Kojic Acid ◽  
Normal Growth ◽  
Competitive Inhibitor ◽  
Inhibitory Effect ◽  
Pupal Weight ◽  
Mrna Levels ◽  
Melanin Biosynthesis ◽  
Horticultural Pest ◽  
Inhibition Experiment

AbstractPhenoloxidase (PO) plays a key role in melanin biosynthesis during insect development. Here, we isolated the 2310-bp full-length cDNA of PPO1 fromZeugodacus tau, a destructive horticultural pest. qRT-polymerase chain reaction showed that theZtPPO1transcripts were highly expressed during larval–prepupal transition and in the haemolymph. When the larvae were fed a 1.66% kojic acid (KA)-containing diet, the levels of theZtPPO1transcripts significantly increased by 2.79- and 3.39-fold in the whole larvae and cuticles, respectively, while the corresponding PO activity was significantly reduced; in addition, the larval and pupal durations were significantly prolonged; pupal weights were lowered; and abnormal phenotypes were observed. Anin vitroinhibition experiment indicated that KA was an effective competitive inhibitor of PO inZ. tau. Additionally, the functional analysis showed that 20E could significantly up-regulate the expression ofZtPPO1, induce lower pupal weight, and advance pupation. Knockdown of theZtPPO1gene by RNAi significantly decreased mRNA levels after 24 h and led to low pupation rates and incomplete pupae with abnormal phenotypes during the larval-pupal interim period. These results proved that PO is important for the normal growth ofZ. tauand that KA can disrupt the development of this pest insect.

scholarly journals Inhibition against CFU-C and CFU-E colony formation by soluble factor(s) derived from hairy cells

Blood ◽  
1989 ◽  
Vol 73 (4) ◽  
pp. 907-913 ◽  
Author(s):  
N Taniguchi ◽  
H Kuratsune ◽  
A Kanamaru ◽  
Y Tokumine ◽  
S Tagawa ◽  
...  
Keyword(s):  
Conditioned Medium ◽  
Colony Formation ◽  
Inhibitory Effect ◽  
Lymphocytic Leukemia ◽  
Hairy Cell ◽  
Cell Leukemia ◽  
Hairy Cells ◽  
Cell Conditioned Medium ◽  
Normal Controls

Abstract The inhibitory effect by hairy cell conditioned medium (HCCM) on the growth of granulocyte and erythrocyte colony forming cells was studied in vitro. The percent inhibition of CFU-C formation by HCCM from four hairy cell leukemia (HCL) patients ranged from 36% to 76%, while no inhibition was observed with conditioned medium (CM) obtained from three B-cell chronic lymphocytic leukemia (B-CLL) patients nor from two normal controls. HCCM inhibited specially the growth of rG-CSF responding stem cells. The hairy cell-derived colony inhibitory factor from HCCM was nondialyzable, fairly stable to heat treatment, and trypsin sensitive. Its maximal inhibitory activity against granulopoiesis was observed in the fractions of 5,000 to 6,000 daltons. Moreover HCCM inhibited CFU-E colony formation but not BFU-E. These results indicate that hairy cells produce a factor that inhibits granulopoiesis and erythropoiesis in vitro. This factor may play a role in neutropenia and anemia observed in HCL.

Effect of Ethanol on Erythrocyte Acetylcholinesterase Activity

1986 ◽  
Vol 23 (4) ◽  
pp. 458-462 ◽  
Author(s):  
Nuha A Haboubi ◽  
D I Thurnham
Keyword(s):  
Ache Activity ◽  
Acetylcholinesterase Activity ◽  
Inhibitory Effect ◽  
In Vitro Experiments ◽  
Previous Exposure ◽  
Organophosphorus Poisoning ◽  
The Mean ◽  
Erythrocyte Ache ◽  
Early Indication

Erythrocyte acetylcholinesterase (AchE) activity was measured in the blood of 36 alcoholic subjects and 41 healthy volunteers. The mean activity in the alcoholics was significantly lower than that in the control subjects. In vitro experiments showed that ethanol inhibited the AchE activity immediately and in proportion to the concentration of ethanol used. Incubation times up to 6 h did not increase the inhibition significantly. Incubation of normal red cells with ethanol for 15 h, followed by washing, showed also that AchE activity was inhibited by the previous exposure to ethanol and that washing did not reduce the inhibitory effect. The possibility is considered that depressed erythrocyte AchE activity may be an early indication of potential disturbances of the autonomic nervous system. The importance of reporting ethanol intake in patients with organophosphorus poisoning is stressed.

scholarly journals The Inhibitory Effect of Clindamycin onLactobacillus in vitro

2001 ◽  
Vol 9 (4) ◽  
pp. 239-244 ◽  
Author(s):  
Alla Aroutcheva ◽  
Jose A. Simoes ◽  
Susan Shott ◽  
Sebastian Faro
Keyword(s):  
Minimum Inhibitory Concentration ◽  
Inhibitory Concentration ◽  
Inhibitory Effect ◽  
Bacteriostatic Effect ◽  
The Mean ◽  
High Concentrations ◽  
Effect On Growth

Objective:To evaluate thein vitroeffect of varying concentrations of clindamycin onLactobacillusspp.Methods: Concentrations of clindamycin ranging from 1.95–20 000 mg/ml were studied for their effect on the growth of six strains ofLactobacillus.Results:Clindamycin concentrations between 1.95–31.25 mg/ml had no statistically significant effect on growth of lactobacilli (p> 0.05). Concentrations 125 and 250 mg/ml had a bacteriostatic effect. The mean minimum inhibitory concentration (MIC) for studiedLactobacillusstrains was determined as 1000 mg/ml.Conclusion:High concentrations of clindamycin achieved in the vagina by intravaginal application might be inhibitory forLactobacillus.

scholarly journals BMP-4 inhibits follicle-stimulating hormone secretion in ewe pituitary

2005 ◽  
Vol 186 (1) ◽  
pp. 109-121 ◽  
Author(s):  
M-O Faure ◽  
L Nicol ◽  
S Fabre ◽  
J Fontaine ◽  
N Mohoric ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mrna Expression ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Hormone Secretion ◽  
Inhibitory Effect ◽  
Type I ◽  
Mrna Levels ◽  
Dependent Manner

Activins and inhibins, members of the transforming growth factor-beta family are able to stimulate and inhibit, respectively, FSH synthesis and release. Other members of this superfamily, the bone morphogenetic proteins (BMPs), may also affect FSH synthesis in the mouse. The aim of this work was to determine whether BMPs are expressed in the ovine pituitary and whether they play a role in the regulation of FSH release. The mRNAs encoding BMP-2, BMP-4, BMP-7 and the oocyte-derived growth factor, growth differentiation factor (GDF)-9 were detected in the pituitaries of cyclic ewes by reverse-transcriptase PCR, as well as the mRNAs encoding the BMP type I receptors, BMPR-IA (activin-receptor-like kinase (ALK)-3) and BMPR-IB (ALK-6), and type II receptors (BMPR-II). Immunolabeling of pituitary sections revealed the presence of BMPR-IA (ALK-3) and BMPR-II in gonadotrope cells. To investigate the potential effects of BMPs on FSH secretion, ewe pituitary cell cultures were treated with BMP-4 (10−11 M to 10−9 M) for 48 h. Interestingly, FSH release was decreased in a dose-dependent manner. At 10−9 M BMP-4 both FSH concentration and FSHβ mRNA expression were reduced by 40% of control values. In contrast, there was no inhibitory effect on either LH or LHβ mRNA expression. A similar result was found with BMP-6. BMP-4 triggered the phosphorylation of Smad1, suggesting that the effect of BMP-4 on FSH secretion is due to the activation of the BMPs signaling pathway. Furthermore, BMP-4 blocked the stimulatory effect of activin on both FSH release and FSHβ mRNA and amplified the suppression of FSH release and FSHβ mRNA levels induced by 17β-estradiol. These results indicate that a functional BMP system operates within the sheep pituitary, at least in vitro, to decrease FSH release and to modulate the effect of activin.

Sox9-dependent transcriptional regulation of the proprotein convertase furin

2007 ◽  
Vol 293 (1) ◽  
pp. C172-C183 ◽  
Author(s):  
Philippe Guimont ◽  
Francine Grondin ◽  
Claire M. Dubois
Keyword(s):  
High Mobility ◽  
Inhibitory Effect ◽  
Nodule Formation ◽  
Mrna Levels ◽  
Paracrine Factor ◽  
Proprotein Convertase ◽  
Hmg Box ◽  
Repressive Effect

The proprotein convertase furin participates in the maturation/bioactivation of a variety of proproteins involved in chondrogenesis events. These include parathyroid hormone-related peptide (PTHrP), an autocrine/paracrine factor that is crucial to both normal cartilage development and cartilage-related pathological processes. Despite the known importance of furin activity in the bioactivation of the polypeptides, the mechanisms that control furin regulation in chondrogenesis remain unknown. To gain insight into the molecular regulation of furin, we used the mouse prechondrogenic ATDC5 cell line, an established in vitro model of cartilage differentiation. Peak expression of both furin mRNA and furin PTHrP maturation was observed during chondrocyte nodule formation stage, an event that correlated with increased mRNA levels of Sox9, a potent high-mobility-group (HMG) box-containing transcription factor required for cartilage formation. Inhibition of furin activity led to a diminution in maturation of PTHrP, suggesting a relationship between Sox9-induced regulation of furin and chondrogenesis events. Transient transfection of Sox9 in nonchondrogenic cells resulted in a marked increase in furin mRNA and in the transactivation of the furin P1A promoter. Direct Sox9 action on the P1A promoter was narrowed down to a critical paired site with Sox9 binding capability in vitro and in vivo. Sox9 transactivation effect was inhibited by L-Sox5 and Sox-6, two Sox9 homologs also expressed in ATDC5 cells. Sox6 inhibitory effect was reduced when using Sox6-HMG-box mutants, indicating a repressive effect through direct HMG-box/DNA binding. Our work suggests a mechanism by which furin is regulated during chondrogenesis. It also adds to the complexity of Sox molecule interaction during gene regulation.

scholarly journals Role of CD40 Ligand in Mycobacterium avium Infection

1999 ◽  
Vol 67 (7) ◽  
pp. 3558-3565 ◽  
Author(s):  
Tomoko Hayashi ◽  
Savita P. Rao ◽  
Pascal R. Meylan ◽  
Richard S. Kornbluth ◽  
Antonino Catanzaro
Keyword(s):  
Mycobacterium Avium ◽  
Human Monocyte ◽  
Opportunistic Pathogen ◽  
Cd40 Ligand ◽  
Inhibitory Effect ◽  
Interleukin 12 ◽  
Intracellular Growth ◽  
Cell Counts ◽  
Avium Infection

ABSTRACT Mycobacterium avium is a common opportunistic pathogen in immunocompromised patients such as those infected with human immunodeficiency virus. Although M. avium is an intracellular organism replicating predominantly in macrophages, disseminated M. avium infection is seen in AIDS patients with CD4+ cell counts of <50 cells/μl, suggesting a possible involvement of a T cell-macrophage interaction for the elimination of M. avium. To determine whether CD40-CD40 ligand (CD40L) interactions play a role in M. aviuminfection, we studied the ability of CD40L to restrict M. avium replication in human monocyte-derived macrophages (MDM) in vitro. MDM were infected with M. avium and cocultured with CD40L-transfected 293 cells for 7 days. Intracellular growth ofM. avium in these MDM was assessed by colony counting. CD40L-expressing cells inhibited growth of M. avium in MDM by 86.5% ± 4.2% compared to MDM cultured with control cells. These findings were verified by assays using purified, soluble recombinant human CD40L (CD40LT). CD40LT (5 μg/ml) inhibited intracellular growth of M. avium by 76.9% ± 18.0% compared to cells treated with medium alone. Inhibition by CD40LT was reduced by monoclonal antibodies (MAbs) against CD40 and CD40L. The inhibitory effect of CD40LT was not accompanied by enhancement of interleukin-12 (IL-12) production by M. avium-infected MDM, while CD40L-expressing cells stimulated IL-12 production by these cells. Treatment of M. avium-infected mice with MAb against murine CD40L resulted in recovery of larger numbers of organisms (0.8 to 1.0 log) from the spleens, livers, and lungs of these animals compared to infected mice which received normal immunoglobulin G. These results indicate that CD40-CD40L signaling may be an important step in host immune response against M. avium infection.

EFFECTS OF TAMOXIFEN ON THE BINDING AND METABOLISM OF TESTOSTERONE BY HUMAN PROSTATIC TISSUE AND PLASMA IN VITRO

1979 ◽  
Vol 83 (3) ◽  
pp. 369-378 ◽  
Author(s):  
F. K. HABIB ◽  
G. RAFATI ◽  
M. R. G. ROBINSON ◽  
S. R. STITCH
Keyword(s):  
Dehydrogenase Activity ◽  
Reductase Activity ◽  
Hydroxysteroid Dehydrogenase ◽  
Inhibitory Effect ◽  
Prostatic Tissue ◽  
Sex Hormone Binding Globulin ◽  
Benign Tissue ◽  
The Mean ◽  
Malignant Prostate

The in-vitro metabolism of testosterone in benign and malignant prostatic tissue was examined and distinct quantitative differences between the two types of specimens were observed. The major metabolite of testosterone in the hyperplastic prostate was 5α-dihydrotestosterone and a high 3α(β)-hydroxysteroid dehydrogenase activity was also detected. In the malignant tissue, 5α-reductase activity was considerably reduced and there was little or no androstanediol formed; the 17β-dehydrogenase activity was, however, higher than in the benign tissue. The decrease in 5α-reductase was always followed by a compensatory change in the 3α(β)-hydroxysteroid dehydrogenase of the malignant prostate. The present study revealed that the ratio of the mean activities of 5α-reductase to 3α(β)-hydroxysteroid dehydrogenase in the two types of specimen always remained a constant. Although the antioestrogen, tamoxifen, induced an inhibitory effect on the activities of 5α-reductase and 17β-hydroxysteroid dehydrogenase in the gland, the present investigation also suggested that tamoxifen stimulated the activity of 3α(3β)-hydroxysteroid dehydrogenase. In blood, the action of tamoxifen appeared to be confined to the displacement of androgens from the binding sites on the sex hormone binding globulin.

Abstract 305: HDL Antagonizes the Defects in the Lymphatic System that Contribute to the Pathogenesis of Rheumatoid Arthritis

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Radjesh Bisoendial ◽  
Wolfgang Weninger ◽  
Francine Petrides ◽  
Fatiha Tabet ◽  
Paul P Tak ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Density Lipoprotein ◽  
Inhibitory Effect ◽  
Tube Formation ◽  
Mrna Levels ◽  
Long Term Effects ◽  
Hypoxic Conditions ◽  
Therapeutic Benefits ◽  
Erosive Arthropathy

Rheumatoid arthritis (RA) is a common inflammatory erosive arthropathy that increases cardiovascular (CV) risk two-fold. Lymphatic dysfunction, a hallmark of chronic inflammation, is considered an attractive target to resolve synovial inflammation. Given the strong vascular anti-inflammatory properties of high-density lipoprotein (HDL) and its key apolipoprotein (apo)A-I, we hypothesized that they may promote inflammation resolution in RA by improving lymphatic endothelial function via up-regulation of the homeobox-containing transcription factor, Prox-1,a key regulator of inflammation-induced lymphangiogenesis (IIL) . Primary human dermal lymphatic endothelial cells (LEC) were treated for 3 days with TNFα (10 ng/mL) or pre-incubated with apoA-I (1.2 mg/mL) for 24 h, followed by TNFα exposure for 3 days. Prox1 mRNA levels were quantified by qPCR. For the tube formation assay, LECs were seeded into a pre-coated Matrigel 24-well plate, and treated with TNFα for 6 h or pre-incubated with apoA-I for 24 h, followed by TNFα exposure for 6 h. Mouse thoracic ducts (TD) were isolated from 2-4 month old C57Bl/6 mice for studying lymphatic vessel (LV) sprouting. TD rings (1 mm) were implanted into a 3-D culture system containing Matrigel under hypoxic conditions and either treated with TNFα, or pre-incubated for 24 h with apoA-I then exposed to TNFα. Incubation with TNFα decreased LEC Prox1 mRNA levels by about 56% (P<0.05). Prior exposure of LECs to apoA-I blocked TNFα-mediated Prox-1 suppression (P<0.05). TNFα also reduced LEC tube formation by about 55% (p<0.05) and completely inhibited LV sprouting from TD rings (p<0.05). ApoA-I protected against TNFα-mediated inhibition of LEC tube formation (44.7±8.1 versus 81.9±15.0% of control; P<0.05) and the inhibitory effect of TNFα on LV sprouting (P<0.05). These results suggest that apoA-I directly regulates IIL by upregulating Prox1 and protecting against TNFα-mediated restriction of lymphatic sprouting and growth in vitro. Hence, raising HDL may provide dual therapeutic benefits in RA by targeting inflammation and reducing cardiovascular risk. New classes of HDL-raising drugs will allow us to study the long term effects of increasing HDL levels on RA progression and CV risk.

SERENDIPITOUS PROTECTION FROM PLATELET-MEDIATED DISORDERS IN STEROID-TREATED PATIENTS?

1987 ◽  
Author(s):  
H Holloway ◽  
A J Moriarty ◽  
S D Nelson ◽  
K Balnave
Keyword(s):  
Ex Vivo ◽  
Thromboxane A2 ◽  
Treated Group ◽  
Inhibitory Effect ◽  
Platelet Volume ◽  
Counter Model ◽  
The Mean ◽  
Possible Cause ◽  
Endogenous Steroid

The aim of this study is to investigate the influence of exogenous corticosteroids on platelet aggregation. This is widely recognised to be of significance in the pathogenesis of acute myocardial infarction and other vascular/haematological disorders.Blood was taken from a cohort of patients (N = 10) undergoing treatment with ACTH or corticosteroids for varied systemic illness. Ex vivo measurements of platelet parameters were made with a Coulter Counter Model S Plus III on nonanticoagulated blood directly from the circulation. Subsequently, aliquots of anticoagulated blood in batches of five were processed at intervals over 24 hours. For comparison, a similar study was undertaken in normal volunteers not on any medication. The mean percentage changes ± standard deviations over the 24 hour interval in platelet count (PLT), mean platelet volume (MPV) and plateletcrit or biomass (PCT) in the respective groups were as follows:-PLT: -(3.12 ± 2.68) vs -(14.77 ± 3.96)(p < 0.001);MPV: 28.88±8.92 vs 46.68±12.54 (p <0.01);PCT: 25.18 ± 8.16 vs 23.75 ± 8.97 (NS).The in vitro alteration in PCT over 24 hours in both cohorts is similar and is due to platelet swelling. The change in MPV is partly due to swelling and partly due to aggregation as evidenced by the decrease in PLT. The significantly smaller drop in PLT and smaller rise in MPV in the steroid-treated group clearly demonstrate that platelets from these patients are less aggregable. A possible cause is that the inhibitory effect of steroids on phospholipase may lead to reduced levels of thromboxane A2. Thus patients on steroid therapy or with high endogenous steroid levels may enjoy serendipitous protection from a variety of platelet mediated disorders. The work may also explain in part why such patients are more prone to bleeding diatheses.

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