Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bilateral decentralization of the superior cervical ganglia (SCG) reduced the pulmonary inflammation that develops 4-8 h after induction of anaphylaxis in Nippostrongylus brasiliensis-sensitized rats. Histamine levels in peritoneal lavage fluid and rat mast cell protease type II in serum were increased to comparable levels in sham-operated and decentralized rats. In vitro stimulation of alveolar macrophages (ALM) with lipopolysaccharide (LPS) provoked tumor necrosis factor-alpha (TNF-alpha) release that was two to three times greater with unchallenged decentralized rats than with sham-operated rats. However, after allergen challenge LPS-stimulated TNF-alpha release from ALM of sham-operated rats increased threefold and lasted at least 24 h, whereas with decentralized rats release of this cytokine actually decreased at 4 and 8 h. The increase in the phagocytosis and respiratory burst of circulating neutrophils seen at 4 and 8 h after allergen challenge in sham-operated rats was reduced significantly by decentralization. These results suggest that the attenuation of anaphylaxis-induced pulmonary inflammation that occurs with decentralization of the SCG is primarily associated with downregulation of neutrophil and macrophage functions.
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PMID:Temporal analysis of the anti-inflammatory effects of decentralization of the rat superior cervical ganglia. 751 90

We have previously demonstrated the increase of histidine decarboxylase activity and histamine content in the murine hypothalamus after intracerebroventricular injection of lipopolysaccharide possibly due to inducible interleukin-1 beta (IL-1 beta). Therefore, we investigated the effects of IL-1 beta on brain histamine dynamics by directly injecting it into the tuberomammillary nucleus of the rat hypothalamus (TM) using an in vivo microdialysis method. Injection of artificial cerebrospinal fluid or recombinant murine IL-1 beta at 0.1 ng into the TM did not evoke a significant change in core temperature, however, a significant monophasic febrile response was observed following injection of IL-beta at more than 1 ng per animal. Histamine release in the anterior hypothalamic area in vivo was significantly augmented from 140 min to 360 min following injection of IL-1 beta at 10 ng dose. These results suggest the possibility that interrelationship between histamine and IL-1 beta may modulate the acute phase reaction in the central nervous system.
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PMID:Interleukin-1 beta induces histamine release in the rat hypothalamus in vivo. 753 93

Helicobacter pylori is important in the aetiology of peptic ulceration. Despite inducing an inflammatory response in the mucosa, the organism persists, suggesting that it has efficient protective mechanisms. Some bacterial and viral products modulate histamine secretion from inflammatory cells. Therefore, this study examined the modulatory effects of H. pylori preparations on histamine release from rat peritoneal mast cells and human basophils. Eleven clinical isolates of H. pylori were prepared in different ways: as whole washed bacteria, washed sonicated bacteria, and formalin-killed bacteria, and as outermembrane and lipopolysaccharide (LPS) extracts. Histamine release from mast cells or basophils was not elicited by any of these bacterial preparations alone. However, when mixed with various secretory stimulants, the bacterial preparations caused inhibition of histamine release from rat mast cells (calcium ionophore A23187, compound 48/80, concanavalin A, anti-rat IgE) and human basophils (A23187, N-formyl Met-Leu-Phe). The degree of inhibition ranged from 48% to 97%. These results indicate that H. pylori exerts an inhibitory effect on cells of the immune system that contributes to its persistence within the gastric mucosa.
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PMID:Modulatory action of Helicobacter pylori on histamine release from mast cells and basophils in vitro. 754 Jun 93

Histamine may be involved in the regulation of hematopoiesis. However, it remained obscure what kind of cells are responsible for its synthesis in bone marrow (BM). In this study, a pure population of macrophages were raised from BM of W/Wv mice, which are genetically deficient in mast cells. The addition of Escherichia coli lipopolysaccharide (LPS) or murine recombinant granulocyte/macrophage colony-stimulating factor (mrGM-CSF) alone had essentially no effect on histamine synthesis. However, the latter rendered the cells responsive to LPS, leading to a marked increase in HDC-dependent histamine synthesis.
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PMID:Histamine synthesis by bone marrow-derived macrophages. 776 19

Histamine trifluoromethyl-toluidine derivative (HTMT), a novel immunosuppressive agent, stimulates H1, H2 and HTMT receptors in lymphocytes. HTMT receptors are different from the classical H1, H2 or H3 receptors. Stimulation of HTMT receptors results in increased intracellular concentrations of calcium ([Ca2+]i) and inositol phosphate (IP) in human peripheral blood lymphocytes. In the present study, we investigated the effects of lymphokines [interleukin-4 (IL-4), interleukin-2 (IL-2)] and other pharmacologic agents [lipopolysaccharide (LPS), phorbol 12-myristate 13-acetate (PMA)] on HTMT-induced Ca2+ and IP responses in non-rosetted cells. HTMT caused enhanced [Ca2+]i and IP responses when the cells were pretreated with IL-4. The effects of IL-4 were concentration dependent and became maximal after the cells were incubated with IL-4 for 48 hr. Inhibitors of protein synthesis, but not of RNA synthesis, blocked the effects of IL-4 on HTMT-induced responses. LPS was more potent than IL-4 in augmenting CA2+ mobilization induced by HTMT. However, the effects of LPS were not altered by inhibitors of either protein synthesis or RNA transcription. This indicated that LPS may act differently than IL-4 on the HTMT response. IL-2 and PMA did not affect HTMT-induced [Ca2+]i and IP responses. The effects of IL-4 and LPS were agonist specific. They did not affect the Ca2+ mobilization induced by PAF. The data indicate that the response to HTMT can be regulated by IL-4 and LPS. Although the in vivo importance of these receptors is not yet clear, the receptor is likely a contributor to immune and/or inflammatory regulation.
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PMID:Effects of lymphokines and mitogens on a histamine derivative-induced intracellular calcium mobilization and inositol phosphate production. 801 Sep 95

Promyelocytic HL-60 cells differentiated into mature cells when they were cultured in the presence of dimaprit (10(-4) M), a histamine H2 agonist. An injection of Escherichia coli lipopolysaccharide increased the activity of histidine decarboxylase in bone marrow cells in C3H/HeN mice to a much greater extent than in C3H/HeJ mice, which are resistant to various effects of lipopolysaccharide. Histamine production increased concomitantly. In WBB6/F1 (W/W(v)) mice, which are genetically deficient in mast cells, histidine decarboxylase activity increased more than in C3H/HeN mice. Pure (>99% nonspecific esterase, CD14 and Mac-1 positive) macrophage populations were obtained from long-term culture of the bone marrow cells (bone marrow-derived macrophages, BMDM). Culture of the cells in the presence of lipopolysaccharide caused a slight, but dose-dependent increase in histidine decarboxylase-associated histamine synthesis. Granulocyte/macrophage colony-stimulating factor (rmGM-CSF) or interleukin 3 (rmIL-3) potently increased lipopolysaccharide-induced histamine formation.
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PMID:Role of histamine produced by macrophages in mouse bone marrow. 875 Jul 90

A novel technique involving radiolabeled monoclonal antibodies was used to characterize and compare the expression of E- and P-selectin on unstimulated, histamine-challenged, and endotoxin-challenged endothelial cells in various tissues of the mouse. Under unstimulated conditions, E-selectin was absent in all organs, but significant expression of P-selectin was observed in several organs. Histamine induced a rapid time-dependent upregulation of P-selectin, with the largest responses observed in mesentery and lung. Significant fold elevations in P-selectin expression occurred as early as 5 minutes after the histamine injection and remained elevated up to 1 hour. Histamine-induced P-selectin upregulation was inhibited by the H1 receptor antagonist diphenhydramine, whereas the H2 receptor antagonist cimetidine had no effect. Endotoxin (lipopolysaccharide [LPS]) also induced a time-dependent expression of P-selectin that reached a maximum between 4 and 8 hours after endotoxin administration. LPS-induced upregulation of P-selectin was greatest in heart and stomach, which exhibited insignificant constitutive expression of P-selectin. LPS also induced a time-dependent upregulation of E-selectin, with maximal expression occurring 3 to 5 hours after intraperitoneal administration. The lung and small intestine exhibited the largest responses to LPS challenge. Histamine administration did not affect E-selectin expression in any tissue. E- and P-selectin-deficient mice were used to test the specificity of monoclonal antibody binding in unstimulated, histamine-challenged, and LPS-stimulated tissues. Vascular binding of the radiolabeled E-selectin and P-selectin monoclonal antibodies was not observed in the respective deficient mice. These findings suggest that P-selectin is constitutively expressed on vascular endothelium in some tissues of the mouse and that there are significant regional differences in the magnitude and time course of histamine- and endotoxin-induced P-selectin expression. In contrast, E-selectin appears to be absent on unstimulated vascular endothelium but is upregulated within 3 hours after the administration of endotoxin in most tissues.
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PMID:Heterogeneity of expression of E- and P-selectins in vivo. 878 89

Nitric oxide (NO) synthesized by airway epithelium may be important in the regulation of airway inflammation and reactivity. As such, the expression and localization of nitric oxide synthase (NOS) isoforms was assessed in human airway tissue obtained following thoracotomy, and in cultured human airway epithelial (BEAS-2B) cells. NOS expression was determined by reverse transcription-polymerase chain reaction (RT-PCR)/Southern blot analysis, and localized by in situ hybridization and immunohistochemistry. No synthesis by cell cultures was detected by nitrite assay. Endothelial and neuronal constitutive NOS mRNAs were not detected in airways or cell cultures. Inducible NOS (iNOS) mRNA was detected in 5 of 6 airway specimens, and in situ hybridization demonstrated iNOS mRNA expression in columnar epithelial cells. This was confirmed by immunohistochemistry using an iNOS specific antibody. BEAS-2B cell cultures were stimulated with (I) combinations of tumor necrosis factor alpha (TNF alpha) (50-2,000 U/ml)/interferon gamma (IFN gamma) (20-500 U/ml)/lipopolysaccharide (LPS) (10 micrograms/ml) or (2) histamine (10(-3) M-10(-5) M). Cell cultures treated with TNF alpha/IFN gamma/LPS in combination expressed iNOS mRNA, and this was associated with increases in supernatant nitrite concentrations over 24 h; however, this response diminished with successive passage of cells. Histamine treatment did not result in iNOS mRNA expression or detectable NO synthesis. We conclude that iNOS in human airway tissue is localized to the airway epithelium. Cytokine/ LPS stimulation, but not histamine, results in iNOS mRNA expression and NO synthesis in BEAS-2B cells. BEAS-2B cells may not be a suitable model for the study of NO biology in airway epithelium.
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PMID:Expression and activity of nitric oxide synthases in human airway epithelium. 919 64

Tumor necrosis factor alpha (TNF-alpha), a major product of alveolar macrophages (AM), has been implicated in many pulmonary diseases. Histamine, a mediator important in pulmonary inflammation, has been demonstrated to regulate the production of TNF-alpha by monocytes. In this study, we show that human AM and monocytes differ in their responses to histamine. Whereas histamine suppressed lipopolysaccharide (LPS)-stimulated TNF-alpha production by monocytes through a cAMP-dependent mechanism, it had no effect on either cAMP levels or TNF-alpha production by AM. In contrast, both PGE2 and IL-10 suppressed LPS-stimulated TNF-alpha production by AM and monocytes. The lack of response of AM to histamine appears unique, as histamine suppressed LPS-stimulated TNF-alpha production by mononuclear cells isolated from sites of acute and chronic inflammation, as well as from noninflammatory tissues, and by macrophages differentiated in vitro. In the presence of the phosphodiesterase (PDE) inhibitor 3-isobutyl-1-methylxanthine, histamine increased cAMP levels in AM. Freshly isolated monocytes and AM did not differ in PDE activity. However, PDE activity in AM, but not in monocytes, was increased 15 min after culture with histamine and may, in part, be responsible for the inability of histamine to suppress TNF-alpha production by AM. However, this increase was small and we hypothesize that additional mechanisms may contribute to the unresponsiveness of AM to histamine. We suggest that the lack of response of AM to histamine may be important in the host defense function of AM in the distal lung.
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PMID:Inability of histamine to regulate TNF-alpha production by human alveolar macrophages. 927 10

Histamine is considered one of the important mediators of immediate hypersensitivity and inflammation, and acts via G protein-coupled receptors. Here, we report that histamine may affect antigen receptor-mediated immune responses of T and B cells via a signal(s) from histamine H1 receptors (H1Rs). Histamine exhibited enhancing effects on the in vitro proliferative responses of anti-CD3epsilon- or anti-IgM-stimulated spleen T and B cells, respectively, at the culture condition that the fetal calf serum was dialyzed before culture and c-kit-positive cells were depleted from the spleen cells. In studies of histamine H1R knockout mice, H1R-deficient T cells had low proliferative responses to anti-CD3epsilon cross-linking or antigen stimulation in vitro. B cells from H1R-deficient mice were also affected, demonstrating low proliferative responses to B cell receptor cross-linking. Antibody production against trinitrophenyl-Ficoll was reduced in H1R-deficient mice. Other aspects of T and B cell function were normal in the H1R knockout mice. H1R-deficient T and B cells showed normal responses upon stimulation with interleukin (IL)-2, IL-4, CD40 ligand, CD40 ligand plus IL-4, and lipopolysaccharide. Collectively, these results imply that the signal generated by histamine through H1R augments antigen receptor-mediated immune responses, suggesting cross-talk between G protein-coupled receptors and antigen receptor-mediated signaling.
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PMID:Augmentation of antigen receptor-mediated responses by histamine H1 receptor signaling. 998 82


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