A simple method for assessing the binding of concanavalin A to mononuclear cell surfaces: no interference of visceral leishmaniasis serum on this binding

Barral‐Netto, Manoel; Barral, Aldina

doi:10.1590/s0074-02761986000300012

Cited by 5 publications

(4 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…More recently Con Br and DGL have also been shown to induce macrophage activation as measured by spreading and H 2 O 2 production (40). Since Con A was found to bind directly on macrophages (41,42) and TNF-␣ production by bone marrow macrophages was shown to be directly induced by the amebic gal-lectin (43), we investigated whether lectins could directly stimulate NO production by murine peritoneal macrophages. Lectin-stimulated adherent cells do produce NO, although nitrite levels are significantly lower than that observed in unfractionated mononuclear cell cultures.…”

Section: Discussionmentioning

confidence: 99%

Lectin-Induced Nitric Oxide Production

Andrade

Arruda

Barbosa

et al. 1999

Cellular Immunology

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

Lectin-Induced Nitric Oxide Production

Andrade

Arruda

Barbosa

et al. 1999

Cellular Immunology

Self Cite

View full text Add to dashboard Cite

show abstract

“…It has been described that plant lectins are able to release NO production in vivo and in vitro [ 19 ]. NO, PGE 2 and TNF-α have emerged as the major effect molecules of murine macrophage cytotoxicity [ 20 ] and the cytotoxic activity of induced macrophages can be characterized by measuring NO, PGE 2 and TNF-α release [ 21 , 22 , 23 ].…”

Section: Resultsmentioning

confidence: 99%

Purification of a Lectin from Arisaema erubescens (Wall.) Schott and Its Pro-Inflammatory Effects

Liu

et al. 2011

Molecules

View full text Add to dashboard Cite

The monocot lectin from the tubers of Arisaema erubescens (Wall.) Schott has been purified by consecutive hydrophobic chromatography and ion exchange chromatography methods. The molecular weight of this A. erubescens lectin (AEL) was determined to be about 12 kDa by high performance liquid chromatography (HPLC) and sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE) methods. AEL could agglutinate rabbit erythrocytes. The haemagglutination activity of AEL was only inhibited by asialofetuin, while monosaccharide did not react. Rat paw edema and neutrophil migration models were used to investigate the pro-inflammatory activity of AEL. AEL (100 and 200 μg/paw) could induce significant rat paw edema. In addition, AEL (100, 200 and 300 μg/mL/cavity) could induce significant and dose-dependent neutrophil migration in the rat peritoneal cavities. Besides, AEL at doses ranging from 100 to 300 μg/mL/cavity could significantly increase the concentration of nitric oxide (NO), prostaglandin E2 (PGE2) and tumor necrosis factor alpha (TNF-α) in peritoneal fluid. As compared with control animals, 75% depletion in the number of resident cells following peritoneal lavage did not reduce the AEL-induced neutrophil migration. However, pre-treatment with 3% thioglycollate which increased the peritoneal macrophage population by 201%, enhanced the neutrophil migration induced by AEL (200 μg/mL/cavity) (p < 0.05). Reduction of peritoneal mast cell population by chronic treatment of rat peritoneal cavities with compound 48/80 (N-methyl-p-methoxyphenethylamine with formaldehyde) did not modify AEL-induced neutrophil migration. The results provided the basis for identifying the toxic components of A. erubescens and AEL could be a new useful tool for pro-inflammatory research.

show abstract

“…Con A in vivo stimulates T cell proliferation and activates macrophages (Deng et al, 1996), either via direct binding to macrophage surface (Barral-Netto and Barral, 1986) or by the activation of lymphocytes. Furthermore, Con A recruits cells to the peritoneal cavity (Rodriguez et al, 1992) and stimulates macrophage nitric oxide (NO) production (Andrade et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Strain differences in concanavalin a-induced paw edema in the rat: Involvement of histamine H1 and H2 receptors

Kuštrimović¹,

Mitić²,

Dimitrijević³

et al. 2011

Acta vet. (Beogr.)

View full text Add to dashboard Cite

The present study tests the hypothesis that the difference in the intensity of paw edema found between the Dark Agouti (DA) and Albino Oxford (AO) rat strains originates from the distinct participation of histamine, serotonin and their corresponding receptors in Concanavalin A (Con A)-induced inflammation. DA and AO male rats were intraplantarly injected with specific receptor antagonists prior to Con A, and the intensity of inflammation was determined by measuring the paw diameter. Our results have showed that histamine H1 and H2 receptor antagonists reduced the Con A-induced paw edema in DA rats, while serotonin 5HT3 receptor antagonist diminished the inflammation in both DA and AO rat strains. The calcium channel blocker did not change Con A-induced inflammation. Strain differences in the intensity and kinetics of inflammation observed between the DA and AO rats are most likely defined by the diversity of mediators released and their receptors activated upon Con A injection

show abstract

A simple method for assessing the binding of concanavalin A to mononuclear cell surfaces: no interference of visceral leishmaniasis serum on this binding

Cited by 5 publications

References 0 publications

Lectin-Induced Nitric Oxide Production

Lectin-Induced Nitric Oxide Production

Purification of a Lectin from Arisaema erubescens (Wall.) Schott and Its Pro-Inflammatory Effects

Strain differences in concanavalin a-induced paw edema in the rat: Involvement of histamine H1 and H2 receptors

Contact Info

Product

Resources

About