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At least 541 records · Page 30Linked to original sources
PubMed2004

Commensal Gram-negative bacteria prime human dendritic cells for enhanced IL-23 and IL-27 expression and enhanced Th1 development.

Dendritic cells (DC) are the main orchestrators of specific immune responses. Depending on microbial information they encounter in peripheral tissues, they promote the development of Th1, Th2 or unpolarized Th cell responses. In this study we have investigated the immunomodulatory effect of non-pathogenic intestinal Gram-negative (Escherichia coli, Bacteroides vulgatus,Veillonella parvula, Pseudomonas aeruginosa) and Gram-positive (Bifidobacterium adolescentis, Enterococcus faecalis, Lactobacillus plantarum and Staphylococcus aureus) bacteria on human monocyte-derived DC (moDC). None of the Gram-positive bacteria (GpB) primed for Th1 or Th2 development. In contrast, despite the low levels of IL-12 they induce, all Gram-negative bacteria (GnB) primed moDC for enhanced Th1 cell development, which was dependent on IL-12 and an additional unidentified cofactor. Strikingly, GnB-matured moDC expressed elevated levels of p19 and p28 mRNA, the critical subunits of IL-23 and IL-27, respectively, suggesting that the IL-12 family members may jointly be responsible for their Th1-driving capacity. Purified major cell wall components of either GnB or GpB did not yield Th cell profiles identical to those obtained with whole bacteria, and could not explain the induction of the IL-12 family members nor Th1 priming by GnB. Importantly, this study gives indications that the expression of the different IL-12 family members is dictated by different priming conditions of immature DC.

Antibodies↗
PubMed1994

Inhibition of PMA-induced human T cell proliferation by bryostatin is associated with enhanced degradation of conventional protein kinase C (cPKC): Ca2+ signals restore mitogenic activity without abrogating enhanced cPKC degradation.

Protein kinase C (PKC)-activating tumor promoters, such as PMA, are mitogenic to human T lymphocytes but, in contrast to many physiological mitogenic agonists, PMA does not operate via a receptor-coupled, IL-2-dependent signaling pathway. Bryostatin, another PKC activator, is not mitogenic to human T cells and, moreover, it inhibits the PMA-induced mitogenic response. Inhibition of the PMA-induced human T cell proliferation by bryostatin correlates with the bryostatin-induced increased degradation rate of conventional PKC (cPKC) isoenzymes. Nevertheless, bryostatin synergizes with suboptimal doses of various T cell mitogens operating via a Ca(2+)-dependent signaling pathway to induce a strong IL-2-dependent proliferative response. Our findings indicate that Ca2+ signals do not abolish the bryostatin-induced enhanced degradation rate of cPKC observed in human T cells. The results suggest that transient activation of cPKC by bryostatin induces some irreversible biochemical events that, by themselves, are not sufficient for the induction of cell proliferation, but that can be complemented by a Ca(2+)-mediated signal(s) leading to IL-2-dependent T cell proliferation. In contrast, PMA-induced IL-2-independent proliferation of human T cells appears to be dependent on the continuous presence of cPKC (that may mediate some critical events at late stages of the response) and, therefore, is inhibited by bryostatin, that induces a rapid degradation of potentially active cPKC.

Biological Transport↗
PubMed1980

Leukocyte migration enhancement as an indicator of immunologic enhancement. III. Common denominators of pregnancy and malignancy.

Leukocyte migration enhancement (LME), a common denominator of pregnancy and malignancy, was investigated in order to determine the immunologic factors and processes involved in this in vitro assay. Reproducibility of results was confirmed by parallel investigations of single patients in an independent laboratory. Preliminary evidence also suggests that the phenomenon of LME is observable not only with the leukocyte migration assay, as performed in the present study, but also with the "indirect" migration inhibitory factor (MIF) assay. Highly significant correlation between results obtained with plasma (PL) and amniotic fluid (AF) was observed (p less than 0.00089). No significant correlation between LME and IgG concentrations as well as complement (C3) concentrations in AF and PL could be detected. C3 concentrations correlated significantly to gravity (p less than 0.007) and parity (p less than 0.003). No immune complexes were detected in either AF or PL samples. An unspecific protein effect as the cause of LME was ruled out in showing no significant correlation between LME and protein concentrations of AF and PL. A highly significant correlation between antigen concentration in PL and migration area was demonstrated (p less than 0.00001). It is suggested that leukocyte migration inhibition (LMI) represents a state of antigen excess, while LME represents antibody excess. Through selective removal of the IgG immunoglobulins LME could be converted into LMI, indicating an IgG subfraction as the responsible immunoglobulin in the phenomenon of LME.

Amniotic Fluid↗
PubMed1980

Leukocyte migration enhancement as an indicator of immunologic enhancement. II. Malignancy.

Leukocyte migration studies were performed on 19 cancer patients and 24 control subjects. Amniotic fluid (AF) as well as autologous plasma (PL) were investigated. No difference in the migration pattern between patients and control subjects was observed with AF, but cancer patients showed significant leukocyte migration enhancement (LME) with PL when compared to control subjects (p less than 0.04). Among 18 cancer patients with persistent disease only three did not show significant LME. All three represented specifically immunodepressed states. None of the untreated group of cancer patients failed to show LME with autologous PL. It is concluded that, as in pregnancy, an immunologic active factor is present in PL of cancer patients which induces a specific subpopulation of leukocytes and thereby LME. The possible mechanism of activation is briefly discussed. Through the detection of LME leukocyte migration may become of importance for the early detection of malignancy and monitoring of treatment success.

Adenocarcinoma↗
PubMed1994

Enhanced immunogenicity of protein-dextran conjugates: I. Rapid stimulation of enhanced antibody responses to poorly immunogenic molecules.

In view of our observation that anti-immunoglobulin antibody conjugated to high-molecular-weight dextran stimulates high levels of B-cell activation (Brunswick et al. J. Immunol. 1989, 143, 1239), we coupled T cell-dependent antigens to dextran. When mice were immunized, in the absence of adjuvant, with a BSA-dextran conjugate (BSA-dex), a persistent, high-titre anti-BSA IgG1 response was induced. Titres were dose-dependent and seen with as little as 10 micrograms of conjugated protein. Anti-BSA titres were detected as early as day 7, usually peaked at about day 14 and persisted for at least 4 weeks. Anti-hapten antibodies were also elicited in mice that were immunized with haptenated BSA covalently bound to dextran, and secondary responses could be induced even after inoculation of the unconjugated protein. Covalent attachment of the protein to the polymer was necessary, and the response was specific, as coinjection of BSA-dex and an unrelated antigen, goat IgG, did not elicit detectable anti-goat antibodies. The immunogenic potential of these conjugates did not depend on the ability of the dextran carrier to induce antibody, inasmuch as they stimulated high levels of anti-protein antibody in mice unresponsive to dextran. A minimum size dextran polymer was required for enhanced immunogenicity as conjugates of BSA with dextran of molecular mass 500 or 2000 kDa but not of 70 kDa gave detectable anti-BSA titres.

Adjuvants, Immunologic↗
PubMed2005

Tramadol enhances hepatic insulin sensitivity via enhancing insulin signaling cascade in the cerebral cortex and hypothalamus of 90% pancreatectomized rats.

Clinical observation found that tramadol, mu opioid receptor (MOR) agonist and serotonin (5-HT) reuptake inhibitor, has a hypoglycemic effect in type 2 diabetes patients. The mechanism of its hypoglycemic effect has not been fully defined. This study showed that tramadol activated a neuronal insulin signaling cascade by increasing the induction of insulin receptor substrate-2 expression in primary cultured neuronal cells while this activation was suppressed by naloxone (MOR inhibitor) and dexamethasone (non-specific inhibitor of MOR and 5-HT receptor, DEX). Glucose utilization of the cerebral cortex and hypothalamus was enhanced by a 4-week-tramadol administration in 90% pancreatectomized rats, in vivo, as assessed by measurement of glucokinase expression and glycogen deposition via activating insulin signaling cascade such as neuronal cells in vitro. This improvement was almost completely suppressed by naloxone as well as DEX. Tramadol decreased fasted serum glucose levels, favored an increase in the glucose infusion rate and reduced endogeneous hepatic glucose production after 4 weeks of treatment. However, tramadol did not modulate hepatic glucose output directly, as exhibited by liver perfusion, suggesting tramadol altered hepatic glucose utilization through the effect of organs other than the liver, possibly the central nervous system. The data suggest that tramadol ameliorates peripheral glucose metabolism through central activation of MOR, and that central and peripheral glucose metabolism are therefore likely to be interrelated.

Animals↗
PubMed2026

Enhancement flavor quality in Zhao'an Baxian oolong tea through enhanced turning-over process.

A systematical investigation on the effects of turning-over intensity on the flavor formation of Zhao'an Baxian oolong tea (ZBT) was performed, through a comparative analysis of heavy turning-over (HT) and light turning-over (LT) treatments in this study. The tea samples were subjected to proteomic and metabolomic analyses, combined with quantitative descriptive analysis (QDA) and electronic sensory (E-tongue/E-nose) evaluation. The results demonstrate that HT significantly reduced the content of bitter and astringent compounds, such as catechins and flavonol glycosides, while promoting the accumulation of umami-related amino acids. Concurrently, HT enhanced the biosynthesis of key floral and fruity volatiles, such as β-ocimene, geraniol, benzaldehyde, jasmone by activating stress-responsive metabolic pathways. These coordinated biochemical changes, driven by enzyme-catalyzed reactions in response to prolonged mechanical wounding and environmental stress, collectively improved the overall sensory profile of ZBT. These findings provide a mechanistic foundation for improving ZBT production, with clear implications for quality control and flavor-oriented product development.

Tea↗
PubMed2006

Immune-enhancing diet and cytokine expression during chronic sepsis: an immune-enhancing diet containing L-arginine, fish oil, and RNA fragments promotes intestinal cytokine expression during chronic sepsis in rats.

Chronic feeding with enteral immune-enhancing diets (IEDs) provides benefits based on composition of the diet, route of feeding, and timing of feeding in relation to timing of trauma or surgery. Our prior studies of acute feeding in naïve rats demonstrated that IED promotes blood flow and proinflammatory cytokines in the ileum. We hypothesized that chronic feeding with IED would shift gut immune status to an anti-inflammatory state during chronic sepsis, resulting in an altered state of cytokine expression in the gut. Five days prior to feeding, gauze was implanted subcutaneously in the backs of male Sprague-Dawley rats, which were fed for 3 days with either control diet (CD, Boost; Mead-Johnson, Evansville, IL) or IED (Impact; Novartis) and randomly assigned to one of four groups: saline control (NS) + control diet (CD), sepsis (EC) + CD, NS + IED, or EC + IED. EC rats were inoculated with 10(9) CFU Escherichia coli and 10(9) CFU Bacteroides fragilis in 2 ml normal saline into the back sponge while NS rats received 2 mL normal saline alone. After 3 days, animals were anesthetized and gut tissue samples were harvested and frozen at -80 degrees C. Tissue protein was extracted and ELISA was performed for interleukin (IL-1beta, IL-5, IL-6, IL-10, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma. In saline controls, IED feeding decreased IL-1beta, IL-5, IL-6, TNF-alpha, and IFN-gamma and increased IL-10 compared with CD-fed animals. In septic animals, IED feeding increased IL-5 and IL-6, while decreasing IFN-gamma and IL-10 in the distal third of the small intestine compared with CD-fed septic rats, whereas IL-1beta and TNF-alpha levels were unchanged. Chronic IED feeding produced a anti-inflammatory state via decreased IFN-gamma and increased IL-5 and IL-6, which both promote gut IgA class switching, suggesting that the gut is shifted toward humoral immunity during chronic IED feeding in septic rats.

Animals↗
PubMed2005

Mouse brain localization of the protein kinase C-enhanced phosphatase 1 inhibitor KEPI (kinase C-enhanced PP1 inhibitor).

We recently identified the protein kinase C-enhanced protein phosphatase 1 (PP1) inhibitor KEPI based on its morphine-induced upregulation in striatum. Regulation of protein serine/threonine dephosphorylation by PP1 can modulate important brain signaling pathways. To improve understanding of KEPI's role in the brain, we have developed anti-KEPI sera in rabbits immunized with a hemocyanin conjugate of KEPI residues 66-80, characterized the specificity that this serum provides, mapped the distribution of immunoreactive KEPI (iKEPI) in mouse brain, rat dorsal root ganglia and striatal cultures and documented KEPI binding to PP1 in vitro. Staining is found in apparently neuronal processes and, often less intensely, in neuronal perikarya in primary cultures and in neurons and neuronal elements from a number of brain regions. iKEPI fiber/terminal patterns are relatively densely distributed in striatum, nucleus accumbens, septum, bed nucleus of the stria terminalis, hippocampus, paraventricular thalamus, ventromedial hypothalamus, interpeduncular nucleus, raphe nuclei, nucleus caudalis of the spinal tract of the trigeminal and dorsal horn of the spinal cord. iKEPI-positive cell bodies lie in the nucleus accumbens, striatum, lateral septal nucleus, granular layer of dentate gyrus, interpeduncular nucleus, dorsal root ganglia and cerebellar vermis. These expression patterns point to possible roles for KEPI in regulating protein dephosphorylation by inhibiting PP1 activities in a number of brain pathways likely to use several different neurotransmitters and to participate in a number of brain functions. Dense KEPI immunoreactivity in nucleus accumbens perikarya, combined with evidence for its regulation by opiates, supports possible roles for KEPI in molecular signal transduction pathways important for drug reward and addiction.

Amino Acid Sequence↗
PubMed2004

Axotomized mouse retinal ganglion cells containing melanopsin show enhanced survival, but not enhanced axon regrowth into a peripheral nerve graft.

Melanopsin is found in only approximately 2% of mouse retinal ganglion cells (RGCs), making these RGCs uniquely and directly photosensitive. Given that the majority of RGCs die after axotomy and that grafting of a peripheral nerve to the eye provides a permissive environment for axon regrowth, the present study examined the survival and axonal regrowth of melanopsin-containing RGCs in mice. One month after optic nerve transection and grafting, RGCs with regrown axons were labeled from the grafts and retinae were processed to visualize melanopsin and TUJ1. Melanopsin-positive and negative RGCs were counted and compared to axotomized RGCs from ungrafted eyes and uninjured RGCs. Melanopsin-positive RGCs showed a 3-fold increase in survival rate compared to non-melanopsin RGCs. Despite this enhanced survival, melanopsin-containing RGCs did not show increased axon regrowth into nerve grafts.

Animals↗
PubMed2002

Analysis of immunoregulatory T-helper cell subsets in patients with multiple sclerosis: relapsing-progressive course correlates with enhanced T H1, relapsing-remitting course with enhanced T H0 reactivity.

In this study, we analysed the recall antigen-induced cytokine production by peripheral blood mononuclear cells (PBMC) from 31 patients with multiple sclerosis (MS) with a relapsing-remitting (rr) and a relapsing-progressive (rp) course and from 40 healthy controls. Cells were stimulated with purified protein derivative (PPD; type 1 response) and tetanus toxoid (TT; type 2 response). Cytokines were determined in the supernatants by ELISA. One of the interesting findings was that healthy controls showed more frequently an IL-5 production after incubation with TT than MS-patients (68% vs.37%; p<0.01), while the type 1 reactivity was only slightly enhanced in MS patients as compared to the controls. However, within the MS patients, there was a significant difference in the incidence of the type 1 reactivity comparing patients with an rp and an rr course (60% vs. 24%; p<0.05). Furthermore, the frequency of a type 0 profile (simultaneous PPD-induced IFN-gamma and TT-induced IL-5 production) was fourfold higher in rr than in the rp patients (43% vs. 10%, p<0.05). In vitro analysis of cytokine profiles in MS could therefore be an interesting approach to evaluate the prognosis of MS (rr vs. rp) already at the beginning of the disease. Thus, it seems that the presence of a type 0 profile is a valid indicator for a favorable course, while a type 1 profile is rather associated with rp MS.

Adult↗
PubMed2006

Surface-enhanced hyper-Raman spectra and enhancement factors for three SERS chromophores. SEHRS spectra on Ag films at pulse energies below 2 pJ.

Hyper-Raman scattering, the nonlinear (two-photon excited) analogue of ordinary Raman scattering, is usually considered to be a weak process that requires high-energy pulsed laser excitation. The sensitivity can be improved greatly by making use of two-photon electronic resonance and/or electromagnetic field enhancement on metal nanoparticle surfaces. Here we demonstrate that hyper-Raman spectra can be obtained from organic dyes on silver colloidal nanoparticle films at laser powers below 1 mW of average power (pulse energies below 2 pJ). These results open the door to exploiting the potential advantages of hyper-Raman scattering for analytical applications.

Carbocyanines↗
PubMed2003

Translational control and metastatic progression: enhanced activity of the mRNA cap-binding protein eIF-4E selectively enhances translation of metastasis-related mRNAs.

To form metastases, tumors must break from the primary tumor site, invade surrounding tissues, enter and survive within the circulation and ultimately colonize a distal tissue. Each of these steps requires the cooperative function of numerous proteins--proteins that facilitate angiogenesis (e.g., VEGF), cell survival (e.g., Bcl-2), invasion (e.g., MMPs), and autocrine growth stimulation (e.g., c-myc, cyclin D1). Although expression of these proteins is regulated at many levels by disparate stimuli, translation of these key malignancy-related proteins is regulated primarily by the activity of the mRNA cap-binding protein eIF-4E, the rate-limiting member of the eIF-4F translation initiation complex. By binding the cap structure at the 5' terminus of cellular mRNAs, eIF-4E recruits mRNAs to the eIF-4F complex, which then scans from the 5' cap through the untranslated region (5'UTR), unwinding secondary structure to reveal the translation initiation codon and to enable ribosome loading. Messenger RNAs with short unstructured 5' UTRs are more easily translated than mRNAs harboring lengthy, highly structured 5' UTRs, as these prohibit efficient scanning and start codon recognition. As such, the translation of these mRNAs, which typically encode proteins involved in angiogenesis (e.g., VEGF), tumor growth (cyclin D1) and survival (Bcl-2), is suppressed except when eIF-4E is engaged with the eIF-4F complex--a common event in many human and experimental cancers. This review focuses on the hypothesis that enhanced eIF-4E function contributes to metastatic progression by selectively upregulating the translation of key malignancy-related proteins that together conspire to drive the metastatic process.

Animals↗
PubMed2003

TH2 Cytokine-enhanced and TGF-beta-enhanced vascular endothelial growth factor production by cultured human airway smooth muscle cells is attenuated by IFN-gamma and corticosteroids.

BACKGROUND: T(H)2 and T(H)1 cytokines have opposite effects on many aspects of the inflammatory response. METHODS: This study was designed to determine if cytokines possibly present in asthma can modulate airway smooth muscle cell (ASMC) production of vascular endothelial growth factor (VEGF) and thus contribute to altered airway vascularity. ASMC were incubated for 24 hours with various concentrations of T(H)2 cytokines (IL-4, IL-5, IL-10, and IL-13); transforming growth factor (TGF)-beta1, TGF-beta2, or TGF-beta3; and IL-1beta or TNF-alpha with or without IFN-gamma. Budesonide and exogenous prostaglandin (PG)E(2) were also evaluated. Postculture media were assayed for VEGF and PGE(2) by ELISA. RESULTS: IL-4, IL-5, and IL-13 alone but not IL-10 enhanced VEGF production by ASMC in a concentration-dependent manner. IFN-gamma alone inhibited spontaneous VEGF release by ASMC and concentration-dependently attenuated IL-4-augmented, IL-5-augmented, or IL-13-augmented production of VEGF (P <.01). All three TGF-beta isoforms augmented VEGF production, which was reduced by IFN-gamma (P <.005). IL-1beta also increased VEGF production, but this was not affected by IFN-gamma (P >.05). TNF-alpha alone had little effect on VEGF release by ASMC. Production of VEGF stimulated by all cytokines was inhibited by budesonide. Exogenous PGE(2) increased VEGF release, but cytokine modulation of PGE(2) release did not always correlate with VEGF release. CONCLUSIONS: T(H)2 cytokines and TGF-beta stimulate ASMC release of VEGF. This can be inhibited by IFN-gamma and glucocorticoids.

Anti-Inflammatory Agents↗
PubMed1997

VMAT2 knockout mice: heterozygotes display reduced amphetamine-conditioned reward, enhanced amphetamine locomotion, and enhanced MPTP toxicity.

The brain vesicular monoamine transporter (VMAT2) pumps monoamine neurotransmitters and Parkinsonism-inducing dopamine neurotoxins such as 1-methyl-4-phenyl-phenypyridinium (MPP+) from neuronal cytoplasm into synaptic vesicles, from which amphetamines cause their release. Amphetamines and MPP+ each also act at nonvesicular sites, providing current uncertainties about the contributions of vesicular actions to their in vivo effects. To assess vesicular contributions to amphetamine-induced locomotion, amphetamine-induced reward, and sequestration and resistance to dopaminergic neurotoxins, we have constructed transgenic VMAT2 knockout mice. Heterozygous VMAT2 knockouts are viable into adult life and display VMAT2 levels one-half that of wild-type values, accompanied by smaller changes in monoaminergic markers, heart rate, and blood pressure. Weight gain, fertility, habituation, passive avoidance, and locomotor activities are similar to wild-type littermates. In these heterozygotes, amphetamine produces enhanced locomotion but diminished behavioral reward, as measured by conditioned place preference. Administration of the MPP+ precursor N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to heterozygotes produces more than twice the dopamine cell losses found in wild-type mice. These mice provide novel information about the contributions of synaptic vesicular actions of monoaminergic drugs and neurotoxins and suggest that intact synaptic vesicle function may contribute more to amphetamine-conditioned reward than to amphetamine-induced locomotion.

Amphetamine↗
PubMed1990

Influenza A virus enhances basophil histamine release and the enhancement is abolished by carbohydrates.

Basophil histamine release was studied in leukocyte suspensions from normal individuals and from patients allergic to house dust mite or birch pollen. Mediator release caused by IgE-mediated reactions was examined by stimulating the cells with anti-IgE or specific antigens, and the calcium ionophore A23187 was used for a non-immunological histamine release. In all experiments influenza A virus caused a synergic enhancement of the mediator release and the potentiation was abolished by galactose (10(-7) to 10(-6) M) and by 10(-6) to 10(-5) M of N-acetylglucosamine, alpha-methyl-D-glucoside, alpha-methyl-D-mannoside, N-acetylneuraminic acid and lactose, but not by glucose. Wash-out experiments show that the sugars prevent the aggravation of mediator release by a binding of sugar to the basophil cell membrane, thereby causing a blockade of binding sites responsible for the potentiating effect of virus.

Adult↗
PubMed1992

Enhanced cell-free transcription of the ribosomal protein L32 gene by the polyoma virus enhancer PEA3 DNA-binding protein.

The mouse-ribosomal-protein-L32-gene promoter contains a 12-bp sequence motif within the 5'-upstream region termed the beta element which shows significant similarity with the consensus sequence of the polyoma-virus-enhancer PEA3. A cloned PEA3 DNA-binding protein, expressed in Escherichia coli and purified, activates the expression of the ribosomal-protein-L32 gene in a cell-free system. Moreover, the PEA3 protein participates in the formation of the ribosomal-protein-L32-promoter-preinitiation-transcription complex. The preinitiation complex formed with PEA3 is resistant to competition by oligonucleotides containing the beta element. In addition anti-PEA3 serum interacts with a factor in mouse L1210 nuclear extract that binds to the beta element, causing a supershift in a mobility-shift assay. Our study demonstrates for the first time that the PEA3 protein can transactivate a cellular gene in a cell-free transcription system.

Animals↗