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)

BALB/c mice infected with Leishmania mexicana developed a chronic infection usually accompanied by the appearance of metastatic lesions. Throughout the 20 weeks of observation, infected mice ;howed an impairment in both in vivo delayed hypersensitivity response and in vitro lymphocyte reactivity to leishmanial antigen. Four to 8 weeks after inoculation infected mice displayed a transitory enhancement of spleen cell responses to phytohemagglutinin P, concanavalin A, and lipopolysaccharide. At the same time, immunization with sheep erythrocytes resulted in a greater number of immunoglobulin P, lipopolysaccharide, and sheep erythrocytes diminished progressively, whereas reactivity to concanavalin A was markedly augmented. When cocultivated with spleen cells from mice infected for 12 to 20 weeks, normal lymphocyte responses to phytohemagglutinin P, concanavalin A, and lipopolysaccharide were drastically reduced. These results suggest a role for suppressor cells in chronic experimental cutaneous leishmaniasis.
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PMID:Alterations of the immune response associated with chronic experimental leishmaniasis. 15 79

Two Leishmania strains, AZV (isolated from a typical case of American cutaneous leishmaniasis) and AMP (from a case of diffuse cutaneous leishmaniasis), were studied in C57BL/6 and BALB/c mice. After infection with 10(4) amastigotes of either strain, C57BL/6 mice developed self-resolving lesions lasting 20 to 23 weeks and showed both delayed hypersensitivity response to leishmanial antigen and specific agglutinating antibodies. On the other hand, BALB/c mice infected with 10(4) AZV or AMP amastigotes developed chronic, large, ulcerated lesions and showed impaired cellular and humoral responses to the parasite. When BALB/c and C57BL/6 mice received 10(2) AMP amastigotes, patterns of infection were similar to those observed after inoculation of 10(4) amastigotes. In vitro studies revealed that spleen cells from AZV- or AMP-infected C57BL/6 mice showed an increased DNA-synthetic response to leishmanial antigen, concanavalin A, and phytohemagglutinin. Spleen cells from AZV- or AMP-infected BALB/c mice showed an increased response to concanavalin A and diminished responses to leishmanial antigen, phytohemagglutinin, and lipopolysaccharide.
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PMID:Comparative study of American cutaneous leishmaniasis and diffuse cutaneous leishmaniasis in two strains of inbred mice. 73 Mar 54

The effect of a purified preparation of glycosphingolipids (GSLs) extracted from Leishmania (L.) amazonensis amastigotes on murine lymphocytes was investigated. GSLs inhibited both concanavalin A (Con A)- or lipopolysaccharide-induced [3H]thymidine uptake by normal and immunized BALB/c mouse lymph node cells. The effect of total GSLs was dose dependent. Total GSLs also suppressed the two-way mixed lymphocyte reaction of BALB/c x C57BL/6 cells and the antigen-specific response of immunized mouse cells. Six pure bands as well as a pool containing a mixture of GSLs with five to seven sugar residues separated by a combination of HPLC and preparative HPTLC were tested and shown to be inhibitors of Con A stimulation. These results suggest that parasite glycosphingolipids may play an immunologically relevant role in leishmaniasis.
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PMID:Inhibition of mouse lymphocyte proliferative response by glycosphingolipids from Leishmania (L.) amazonensis. 138 24

Disturbance of T cell-mediated immunity has been reported in acute visceral leishmaniasis (AVL). In a study of 16 patients with AVL, defective production of interleukin-1 (IL-1) by peripheral blood mononuclear cells was demonstrated in response to leishmania antigens, heat-killed Listeria organisms, and lipopolysaccharide when compared to posttherapy values or controls. This global defect in IL-1 production was corrected after successful therapy. Twelve of 16 patients responded with a greater than or equal to 2.5-fold increase in IL-1 production that correlated with clinical cure, P less than .01. Depressed production of tumor necrosis factor (TNF) was leishmania antigen-specific and similarly recovered after therapy. In vitro TNF production during the follow-up period did not correlate with clinical status but high serum levels were associated with AVL. Since T cells are activated by processed antigens presented on class II major histocompatibility molecules and by newly synthesized IL-1, defective IL-1 production may contribute to the immunosuppression observed in AVL.
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PMID:Diminished in vitro production of interleukin-1 and tumor necrosis factor-alpha during acute visceral leishmaniasis and recovery after therapy. 158 28

Murine peritoneal macrophages activated with interferon (IFN)-gamma and lipopolysaccharide (LPS) produce high levels of nitric oxide (NO) and are efficient in killing the intracellular protozoan parasites Leishmania major in vitro. Earlier studies have shown that NO, whose synthesis in murine macrophages is catalyzed by an inducible enzyme NO synthase, plays a major effector role in the host resistance against microbial infection. We now shown that both the NO synthesis and the leishmanicidal activity can be inhibited by prior treatment of the cells with recombinant interleukin 4 (IL4). IL4 treatment had no effect on the binding of IFN-gamma to macrophages but prevented the induction of NO synthase in these cells activated with IFN-gamma and LPS. Since IFN-gamma is produced by murine T helper type-1 (Th1) cells, whereas IL4 is secreted by Th2 cells, these results suggest a novel pathway by which Th2 cells regulate an activity of Th1 cells, namely by inhibiting the induction of NO synthase. These results may also account for the mechanism by which the disease-promoting Th2 cells counteract the host-protective effect of Th1 cells in leishmaniasis and other intracellular parasitic diseases.
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PMID:A possible novel pathway of regulation by murine T helper type-2 (Th2) cells of a Th1 cell activity via the modulation of the induction of nitric oxide synthase on macrophages. 171 84

Wasting and secretion of the catabolic cytokines tumor necrosis factor (TNF)/cachectin and interleukin 1 (IL-1) were assessed in weanling Syrian hamsters infected with Leishmania donovani amastigotes. Whereas the mean weight of uninfected animals increased progressively over 9 weeks, the mean weight of infected animals plateaued at 4-6 weeks and then decreased progressively until death. Splenic mononuclear cells from control hamsters produced 11.3 +/- 8.3 (SD) ng TNF/10(6) mononuclear cells/24 hr. TNF secretion in infected animals was greater than the mean +/- 2 SD of controls in 1 of 3 hamsters at 2 weeks post-infection and in 8 of 9 hamsters at weeks 4-8. The mean TNF secreted by infected animals studied at weeks 4-8 was 371 (range 28-800) ng TNF/10(6) mononuclear cells/24 hr (P = 0.005). Control hamsters produced 7.7 +/- 2.7 pg IL-1/10(6) mononuclear cells/24 hr. At 2 weeks, mononuclear cells from 2 of 3 infected animals secreted amounts of IL-1 greater than the mean +/- 2 SD of controls. All of 8 infected hamsters secreted increased amounts of IL-1 at 4-8 weeks. The mean was 164 (range 17-370) pg IL-1/10(6) mononuclear cells/24 hr (P = 0.002). In comparison to infected animals, mononuclear cells from control hamsters incubated with lipopolysaccharide, 10 micrograms/ml, produced 172.5 ng TNF and 44.6 pg of IL-1/10(6) mononuclear cells/24 hr. The effect of visceral leishmaniasis on food intake was assessed in a separate group of animals housed individually in metabolic cages. Significant reductions in weight and food intake were first observed at 2 and 3 weeks of infection, respectively. By 5 weeks, the food intake of infected animals was 46% that of controls. Syrian hamsters infected with L. donovani provide an excellent model with which to study the mechanism of wasting.
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PMID:Wasting and macrophage production of tumor necrosis factor/cachectin and interleukin 1 in experimental visceral leishmaniasis. 226 69

A study was undertaken on the immunomodulating properties of pentamidine, a diamidine used in the treatment of African trypanosomiasis, pneumocystosis and leishmaniasis. Pentamidine inhibited the ability of mouse splenic lymphocytes to respond to mitogens. In particular inhibition of the B lymphocyte response was observed. At concentrations of 1 microgram/ml (1.7 x 10(-6) M), pentamidine markedly inhibited the response to the B cell mitogen, lipopolysaccharide (LPS), while concentrations of 10 micrograms/ml had to be attained to produce a similar effect on the response to the T cell mitogens phytohaemagglutinin (PHA) and concanavalin A (ConA). Further studies showed that pentamidine was not toxic to either resting or proliferating cells and probably acts by interacting directly with B cells rather than modifying the regulatory cell populations.
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PMID:Selective inhibition of the in vitro murine B lymphocyte response by pentamidine. 315 93

Extraction of whole promastigotes of Leishmania tropica major and L. donovani with a mixture of hexane and isopropanol (3:2) yielded three fractions containing immunological activity: lipids, where the activity was determined by radioimmunoassay; a lipopolysaccharide-like (LPS-like), water-soluble precipitate, where activity was determined both by radioimmunoassay and double gel diffusion, and the phenol: water extract of the lipid-free promastigotes, where activity was followed by double gel diffusion. The use of a solid state, lipid-based radioimmunoassay for detection of leishmanial antigens provided a sensitive measure of their activity with a considerable degree of species and serotype specificity. We found antibodies to leishmanial lipids in sera from immunized rabbits, convalescent mice, and human patients with confirmed cases of cutaneous leishmaniasis or kala azar. There was very little activity in normal human or animal sera. Analysis by SDS-polyacrylamide gel electrophoresis of fractions from promastigotes surface-labeled with galactose oxidase and sodium borotritiate and preliminary immunochemical characterization of the LPS-like antigen showed that it contained galactose, but otherwise differed immunologically and chemically from excreted factor (EF), the best characterized leishmanial antigen.
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PMID:Lipid and lipopolysaccharide-like antigens of Leishmania promastigotes. 400 12

Visceral leishmaniasis (VL) and cutaneous leishmaniasis (CL) are the major parasitic diseases in which the immune system is implicated in pathogenesis. The in vitro production of interleukin (IL)-2, IL-4, IL-6, IL-8, tumor necrosis factor-alpha (TNF alpha), and granulocyte-macrophage colony-stimulating factor (GM-CSF), spontaneously and in response to stimulation of peripheral blood mononuclear cells with anti-CD3, phytohemagglutinin, and lipopolysaccharide, was investigated to determine their importance in VL and CL. Highly enhanced production of IL-4, IL-6, IL-8, and TNF alpha was seen in VL. However, enhanced production of IL-4 and TNF alpha but almost normal production of IL-6 and IL-8 was seen in CL. The highly increased IL-4 production was the most characteristic and common feature of both VL and CL. Of interest, highly deficient GM-CSF production may be implicated in abnormalities in synthesis of hematopoietic lineage of cells in these diseases.
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PMID:Immunoregulatory and proinflammatory cytokine production in visceral and cutaneous leishmaniasis. 793 Jul 2

Intercellular adhesion molecule-1 (ICAM-1, CD54) is a cell-surface glycoprotein which has been shown to play an important role for cell/cell interaction. Little is known about its occurrence in the murine monocyte/macrophage (M phi) lineage; hence, we analyzed ICAM-1 expression in cells and cell lines representing different stages of M phi maturation and studied its regulation during inflammatory activation. Flow cytometric analysis of bone marrow-derived M phi cultured in the presence of M-CSF, of thioglycollate-elicited peritoneal M phi and of M1 myeloblasts differentiated by lipopolysaccharide (LPS) treatment revealed that ICAM-1 is increasingly expressed during monocytic maturation. Accordingly, the myelomonocytic cell lines RMB.TG, WEHI.TG, J774A and P388D, which can be ordered in a linear differentiation sequence, showed increasing levels of ICAM-1 expression. Furthermore, ICAM-1 expression by bone marrow-derived M phi could be up-regulated by tumor necrosis factor-alpha, interferon-gamma and LPS. In two models of murine experimental inflammation, i.e. induction phase of contact hypersensitivity and cutaneous leishmaniasis, which are both dependent on M phi/T cell interaction, M phi expressing ICAM-1 were found to be highly abundant. In addition, it was demonstrated that co-culture of Leishmania maior parasites with bone marrow M phi led to up-regulation of ICAM-1 on these cells. In conclusion, our data clearly demonstrate that ICAM-1 is increasingly being expressed during maturation of murine M phi. Cytokines and inflammatory stimuli modulate M phi ICAM-1 expression as well thus referring to its considerable role during inflammation, e.g. providing accessory or costimulatory signals for T cell activation.
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PMID:Expression of intercellular adhesion molecule-1 by murine macrophages is up-regulated during differentiation and inflammatory activation. 810 78


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