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

Human cord blood lymphocytes were stimulated with trinitrophenyl--polyacrylamide beads (TNP--PAA) in order to induce a primary IgM anti-TNP response. With few exceptions, no anti-TPN response was obtained, whereas peripheral blood lymphomonocytic cells (PBL) from 18-mth-old children were able to respond to TNP-PAA. The addition of lipopolysaccharide (LPS) or of mitomycin-treated adult PBL to cultures of cord blood lymphocytes significantly enhanced their anti-TNP response, thus showing that functional anti-TNP B cell precursors are present in the human neonate.
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PMID:Primary in vitro antibody response in human cord blood lymphocytes. 741 22

Considering that nitric oxide (NO) may be involved in anti-tumoral and anti-parasite lectin effects, in this report we investigated whether lectin induces NO production. Lectins from Canavalia brasiliensis, Dioclea grandiflora, Pisum arvense (PAA), and concanavalin A induced murine peritoneal cells to produce NO in vitro. PAA induced similar levels to that obtained with lipopolysaccharide plus interferon-gamma. NO production by adherent cells was significantly lower than that of unfractionated cells, suggesting a combination of lectin stimuli directly on macrophages and via lymphocyte stimulation. Ex vivo experiments showed that cells stimulated in vivo could maintain NO production in vitro without further stimuli. NO synthesis blockage in vivo can significantly increase cell numbers in draining lymph nodes after lectin injection compared to unblocked controls, suggesting an in vivo association of lectin stimuli and NO production. Taken together these data show that lectins can induce NO production both in vitro and in vivo.
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PMID:Lectin-induced nitric oxide production. 1035 85

E-selectin-targeted contrast enhancement of blood vessels in inflamed tissues was investigated with a new contrast agent, Gd-DTPA-B(sLe(x))A, which was recently obtained by grafting a synthetic mimetic of sialyl-Lewis(x), an E-selectin ligand, onto Gd-DTPA. The pharmacokinetics, biodistribution, and potential to image inflammation by MRI of this E-selectin-targeted contrast agent were evaluated. The inhibition (by 15-34%) produced by Gd-DTPA-B(sLe(x))A on Sialyl Le(x)-PAA-biotin binding to E-selectin confirmed the specific interaction of the new contrast agent with this adhesion molecule. Gd-DTPA-B(sLe(x))A was tested at a dose of 0.1 mmol/kg b.w. on mice and rats in a fulminant hepatitis model induced by the co-administration of D-galactosamine and E. coli lipopolysaccharide. A significant and prolonged contrast enhancement between blood vessels and liver parenchyma was obtained in pathological conditions, which attests to the specificity of the agent for E-selectin. The prolonged vascular residence (48.9 min in hepatitis vs. 29.8 min in healthy animals), as evidenced by the pharmacokinetic characterization, suggests that Gd-DTPA-B(sLe(x))A interacts with the specific receptors expressed during inflammation. The biodistribution of the compound indicates its retention in inflamed liver by both specific mechanisms and nonspecific accumulation due to the necrotic lesions. The same mechanisms are invoked to account for its retention in the spleen.
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PMID:Magnetic resonance imaging of inflammation with a specific selectin-targeted contrast agent. 1579 62