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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pregnant randombred ICR mice were administered 2.5 or 5.0 mg/kg body weight of CdCl2 on day 16 of pregnancy and immune responses of their offspring were tested postnatally. At the age of 4 weeks, proliferative responses of spleen cells to concanavalin A, phytohemagglutinin and lipopolysaccharide and the background proliferation were enhanced in both experimental groups. The activation index was increased only after activation with concanavalin A and lipopolysaccharide in the group treated by the dose 5 mg/kg. The delayed type hypersensitivity to sheep red blood cells after immunization at 4 weeks was decreased. The serum IgM antibody response to sheep red blood cells was increased in the offspring of females treated with the lower dose of cadmium both at week 4 and 8. Activity of peritoneal macrophages (NBT, H2O2) was enhanced at 4 weeks and lowered subsequently. It is concluded that in mice the maternal exposure to a single dose of cadmium results in postnatally manifested deviations of immune functions of their offsprings.
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PMID:Developmental toxicity of cadmium in mice. II. Immunotoxic effects. 181 May 12

The role of cell-mediated immunity in hamsters during treponemal infection appears to involve the activated macrophage. To date, studies have been hindered by the inability to confirm that macrophages exhibit enhanced treponemicidal activity at the infection site. We show that lipopolysaccharide and thioglycollate-treated animals, when inoculated with Treponema pallidum subsp. pertenue, exhibit enhanced clearance of these organisms compared with controls. Macrophages from these infected groups display an enhanced respiratory burst, as detected by NBT reduction, as well as a marked increase in C3b receptor-mediated ingestion activity. Significant changes in these parameters indicate that alterations in macrophage activation are occurring in the infected compartment. Thus the stimulatory agents apparently modify the host's immune responses to promote subsequent reduction of treponemal infection. In addition, hamster peritoneal macrophages demonstrate enhanced activation behavior as a result of exposure to at least two signals, which may be prerequisite for processing this organism efficiently.
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PMID:The participation of activated peritoneal macrophages in Treponema pallidum subspecies pertenue infection in Syrian hamsters. 386 29

Mouse monocytic Mm-A cells are a highly leukemogenic variant line of the monocytic and non-leukemogenic cell line Mm-1, which developed spontaneously from mouse myeloid leukemia M1 cells. Studies were made on whether Mm-A cells could be induced to differentiate further by agents that were effective for inducing differentiation of the parent M1 cells and other leukemic cells. Of the agents tested, butyrate, conditioned medium from concanavalin A-stimulated spleen cells, lipopolysaccharide (LPS) and N6,O2-dibutyryl adenosine 3'5'-cyclic-monophosphate (dbcAMP) significantly stimulated the lysozyme activity of Mm-A cells, which is one of the most characteristic biochemical markers of monocytes and macrophages. Butyrate was the most effective agent for increasing lysozyme production by Mm-A cells; culture with 0.5mM butyrate for 3 days increased lysozyme production by Mm-A cells about 50-fold. Inducers of M1 cell differentiation such as dexamethasone, 1 alpha,25-dihydroxyvitamin D3, arginase, and proteinous inducer did not increase the lysozyme activity. Butyrate also induced NBT reduction and stimulated other differentiation-associated functions, such as expressions of Fc receptors on the cell surface, immune phagocytosis and production of inducer for M1 cell differentiation. Its effect in stimulating differentiation of Mm-A cells was synergistic with that of dbcAMP or LPS. Incubation with butyrate inhibited the proliferation of Mm-A cells, about 0.3mM butyrate causing 50% inhibition. These results indicate that monocytic, leukemogenic Mm-A cells can be induced to differentiate further by butyrate and that the inducers of differentiation of Mm-A cells are markedly different from those of the parent myeloblastic M1 cells.
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PMID:Induction of differentiation of cultured mouse monocytic leukemia cells (Mm-A) by inducers different from those of parent myeloblastic leukemia cells (M1). 393 26

A polysaccharide fraction (PS) was separated by mild hydrolysis from Haemophilus influenzae lipopolysaccharide. This preparation contained glycosyl-galactosyl, rhamnosyl, glucosaminyl and mannosyl residues (molar ratio: 4-1-1-2-2). It was nontoxic and immunogenic and consisted of at least one stable molecular group (fraction A; MW approximately equal to 10(6)) and an association of aggregated units (fraction B;MW approximately equal to 10(4)). This study evaluated the capacity of phagocytosis and quantitative nitroblue-tetrazolium reduction of mouse macrophages in presence of these polysaccharide fractions. After a 24-h incubation period, PS and fraction A, at 1 mg/ml, increased both phagocytosis and reduction potential of mouse peritoneal macrophages by 100%. In contrast, 1-h incubation with PS or fraction A induced a decrease of 50% in phagocytosis but no modification of NBT reduction. An identical incubation with various sugars showed that only mannosyl polymers could significantly decrease this phagocytic process. As in the case of toxic lipopolysaccharides, macrophages responded to a nontoxic preparation obtained from an endotoxin. We confirmed the role of mannosyl residues in recognition of macrophage binding receptors. Moreover, we suggest that this mannose binding ability was dependent on dose, aggregation state and molecular weight of the preparation.U
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PMID:Action of a polysaccharide fraction of Haemophilus influenzae lipopolysaccharide on macrophage: implication of receptor for mannosyl-polysaccharides. 629 79

The effect of cytokines on the proliferation and differentiation of leukemia cells from 5 patients with acute promyelocytic leukemia (APL) was examined. Interleukin-1 beta (IL-1), interleukin-3 (IL-3), granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (G-CSF) augmented uptake of 3H-thymidine into the DNA of APL cells in a dose-dependent manner in all cases. This stimulatory effect was pronounced in some, but not all, cells treated with all-trans retinoic acid (ATRA). However, nitroblue tetrazolium-reducing activity was induced in a concentration-dependent manner by ATRA in all cases. The cytokines greatly enhanced NBT reduction of APL cells treated with ATRA, and a mixture of cytokines was more effective than a single cytokine. Although GM-CSF, IL-3 and IL-1 significantly modulated the ATRA-induced morphological changes, they did not induce CD14 expression, a typical marker of monocytic differentiation. In the presence of ATRA, GM-CSF potentiated production and secretion of tumor necrosis factor-alpha (TNF) in response to lipopolysaccharide, as well as interferon-gamma which is a potent inducer of monocytic differentiation in APL cells. On the other hand, production of TNF in ATRA-treated cells was not affected by G-CSF which significantly enhanced granulocytic differentiation. The effect of cytokines on APL cell differentiation should be considered in ATRA treatment for APL patients. Potentiation of cytokine production in APL cells associated with myelomonocytic differentiation is noteworthy in the pathogenesis of "retinoic acid syndrome".
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PMID:Effect of cytokines on the proliferation and differentiation of acute promyelocytic leukemia cells: possible relationship to the development of "retinoic acid syndrome". 752 Nov 52

We have developed enhanced immunohistochemical protocols for detecting autonomic nerve fibers and splenocyte-associated proteins in rat spleen. This includes norepinephrine-synthesizing enzymes (dopamine-beta hydroxylase (DBH) and tyrosine hydroxylase (TH)), neuropeptide Y (NPY), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), c-fos protein, inducible nitric oxide synthase (iNOS), and the macrophage cell marker ED1. Animals were divided into sham-operated and splenic nerve-sectioned groups for detection of DBH, TH, and NPY. For immunodetection of TNF-alpha, iNOS, IFN-gamma and c-fos, animals were injected IV with saline or 100 microg of lipopolysaccharide (LPS) and were sacrificed at various time intervals post injection. Rats were perfused with 4% paraformaldehyde, spleens removed and cryoprotected, and 50-microm floating sections were cut on a freezing microtome. Immunodetection was performed with various detection systems and substrate/chromogen solutions, and in some cases using pretreatment with proteinase K (PK) for antigen unmasking. PK pretreatment increased immunostaining for DBH, TH, NPY, IFN-gamma, iNOS, and ED1, and the improvement was concentration-dependent. Using NPY immunostaining to index the signal-to-noise ratio for various substrates and detection systems, we found that an alkaline phosphatase detection system with NBT/BCIP as a substrate was the best procedure for light microscopy, whereas the CY3-labeled secondary antibody technique proved optimal for fluorescent microscopy. Surgical transection of the splenic nerve eliminated all nerve fiber staining for DBH, TH, and NPY. TNF-alpha, IFN-gamma, c-fos, and iNOS proteins were observed in the spleen in a time-dependent manner after LPS stimulation. Fluorescent double labeling, visualized with fluorescent confocal scanning laser microscopy, revealed many NPY fibers distributed among the ED1-labeled macrophages. These results demonstrate that immunohistochemistry can be used to index the activational effects of an immune challenge on splenocytes in situ and verifies that splenic immune cells are innervated by the sympathetic nervous system.
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PMID:Enhanced immunohistochemical detection of autonomic nerve fibers, cytokines and inducible nitric oxide synthase by light and fluorescent microscopy in rat spleen. 911 Dec 38

The aims of this study were to assess the possible role of peripheral benzodiazepine receptors (pBZrs)1 in mediating the in vitro effects of carbamazepine (CBZ) on some neutrophil functions in healthy volunteers and to investigate neutrophil function and pBZr expression in patients with epilepsia on CBZ monotherapy for at least 1 year. In vitro CBZ (42-168 microM) concentration-dependently inhibited chemotaxis induced by N-formyl-methionyl-leucyl-phenylalanine (FMLP) or lipopolysaccharide (LPS)-activated human serum. CBZ did not affect random migration, phagocytosis index, phagocytosis frequency, NBT reduction frequency, C. albicans lethality index and resting superoxide production. The pBZr antagonist PK 11195 (1 microM, per se ineffective) reversed the inhibitory effect of CBZ on chemotaxis induced by endotoxin-activated serum or FMLP. The pBZr agonist Ro 5-4864 (10-100 microM) mimicked the effect of CBZ on chemotaxis induced by endotoxin-activated serum or FMLP and had no effect on the other parameters. Neutrophils from epileptic patients on chronic CBZ monotherapy had impaired FMLP- and serum-induced chemotaxis and enhanced expression of pBZrs on neutrophils. These data strongly suggest an involvement of pBZrs in mediating the in vitro effects of CBZ on chemotaxis; furthermore, impairment of the same neutrophil function parameters and overexpression of pBZrs in patients are consistent with the hypothesis of an in vivo interaction of CBZ with pBZrs.
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PMID:Carbamazepine affects neutrophil function through an action on peripheral benzodiazepine receptors. 924 64

The presence of a Tumor Necrosis Factor alpha (TNFalpha)-like molecule has been suggested in fish by biological assays and biological and antigenic cross-reactivities with human TNFalpha. In the present study, whether rainbow trout macrophages produce TNFalpha was examined. Murine recombinant TNFalpha (m-rTNFalpha) was used as the standard mammalian TNFalpha. The supernatants were harvested from trout macrophage culture stimulated with lipopolysaccharide (LPS) and then passed through a Polymyxin B column to remove LPS. Results show that trout macrophage culture supernatants exhibit TNF-like activities. The supernatants significantly enhanced neutrophil migration and macrophage respiratory burst activity as assessed by NBT reduction test. The supernatants were also highly cytotoxic to murine L929 cells, which are known to be sensitive to mammalian TNFalpha. The biological activities of TNF in the trout macrophage culture supernatant was determined as 2.6 U ml(-1) in the presence of actinomycin D. This indicates biological cross-reactivity of trout TNFalpha-like factor on mammalian cells. Moreover, these activities were inhibited by a rabbit anti-mTNFalpha antibody. These results suggest that rainbow trout macrophages produce a TNFalpha-like factor that is similar to the mammalian TNFalpha in functions.
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PMID:Tumor necrosis factor alpha (TNFalpha)-like factor produced by macrophages in rainbow trout, Oncorhynchus mykiss. 1139 91

The effect of formyl chemotactic peptide (fCTP, fMet-Leu-Phe), beta-amyloid peptides (beta-AP, 1-42, 1-16 and 25-35), and bradykinin (BK) on functional activity of phagocytic cells has been investigated. Wheat germ agglutinin (WGA) was also used as a model membrane binding agent of polypeptide nature. Murine monocyte-macrophage cell line J774.2 and normal human blood polymorphonuclear (PMN) cells were used as target phagocytic cells. Their activity was quantitatively estimated by measuring phagocytosis of killed yeast cells. Beta-AP (1-41) maximally stimulated phagocytosis at 0.1 microg/ml, BK--at 1.0 microg/ml, and fCTP--at 2.0 microg/ml. Beta-AP (1-16) and beta-AP (25-35) were inactive in used test-systems. Phagocytosis-inducing activity of beta-AP (1-42) and BK reached maximal levels in 2 h and decreased after 4-6 h of incubation. Phagocytosis numbers were compared with the indicators of phagocytic cell activation, such as absorption of neutral red dye, glucose utilization, production of super-oxide anion (NBT-test) and nitrite accumulation (indicator of NO production). NBT-test, which may be related to the killing ability of phagocytic cells towards the ingested objects, was positive only in stimulated PMN leukocytes, while the nitrite accumulation was detected only in stimulated macrophages. Nitrite accumulation in macrophages was markedly induced by lipopolysaccharide and to a lower extent by 0.5 microg/ml beta-AP (1-42). In high dose (5.0 microg/ml) beta-AP suppressed nitrite accumulation in macrophages stimulated by lipopolysaccharide. Other studied peptides were inactive in inducing nitrite accumulation. Transforming growth factor type beta suppressed phagocytic activity of PMN cells activated by beta-AP or WGA. The anti-inflammatory drugs (indomethacin and L-lysine aescinate) inhibited beta-AP (1-42)-induced phagocytosis. The interrelations between the regulatory pathways of BK, beta-AP and fCTP are discussed.
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PMID:In vitro studies of activation of phagocytic cells by bioactive peptides. 1251 2

In the present study, we investigated the effects and mechanisms of a novel potent antioxidant, octyl caffeate, on the induction of iNOS expression by lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma) in cultured primary rat aortic smooth muscle cells (RASMCs) in vitro and LPS-induced hypotension in vivo. Octyl caffeate (0.1-1.0 microM) exerted a concentration-dependent inhibition of iron-catalyzed lipid peroxidation in rat brain homogenates. Furthermore, octyl caffeate (20, 50, and 100 microM) concentration-dependently diminished the initial rate of superoxide-induced NBT reduction and the enzymatic activity of xanthine oxidase. It also concentration-dependently (1-50 microM) inhibited the NO production, iNOS protein and messenger RNA expressions upon stimulation by LPS (100 microg/mL)/IFN-gamma (100U/mL) in RASMCs. In addition, we found that octyl caffeate did not significantly affect IkappaBalpha degradation stimulated by LPS/IFN-gamma in RASMCs. On the other hand, octyl caffeate (10 and 50 microM) significantly suppressed activation of c-Jun-N-terminal kinase and extracellular signal-regulated kinase. Moreover, octyl caffeate (10mg/kg, i.v.) significantly inhibited the fall in mean arterial pressure stimulated by LPS (7.5mg/kg) in rats. In conclusion, we demonstrate that a novel potent antioxidant, octyl caffeate, significantly ameliorates circulatory failure of endotoxemia in vivo by a mechanism involving suppression of iNOS expression through inactivation of mitogen-activated protein kinases in RASMCs.
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PMID:A novel antioxidant, octyl caffeate, suppression of LPS/IFN-gamma-induced inducible nitric oxide synthase gene expression in rat aortic smooth muscle cells. 1269 79


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