Mediation of inflammatory ascites formation induced by macromolecules in mice.

The first 60-min phase of inflammatory ascites formation was studied by intraperitoneally (i.p.) administered macromolecular inducers: yeast cell wall zymosan binds to specific macrophage receptors, polyethyleneimine (PEI) and concanavalin A (ConA), produces non-covalent cross-links on the surface of various cells, while λ-carrageenan may function as a contact activator.

Contribution of the Kallikrein/Kinin System to the Mediation of ConA-Induced Inflammatory Ascites.

Intraperitoneal administration of concanavalin A (ConA, 25 mg/kg b.w.), a cell-binding plant lectin was used for inducing inflammatory ascites, and potential inhibitors were tested in 1 h and 2.

Modulation of ConA-induced inflammatory ascites by histamine - short communication.

The early phase of the ConA-induced inflammatory ascites was studied, with special reference to histamine. Concanavalin A (ConA), a cell-surface binding lectin was injected i.p.

Suppression of ConA-induced inflammatory ascites by lipopolysaccharide (LPS) in mice.

The effect of pre-treatment with Escherichia coli O83 lipopolysaccharide (LPS) on concanavalin A-induced ascites was examined. The LPS was injected intraperitoneally (i.p.

Interaction of concanavalin a with bacterial lipopolysaccharides in agarose gel.

Binding of fluorescein isothiocyanate-labeled concanavalin A to a series of molecular species of lipopolysaccharide (LPS), purified from pathogenic bacteria, was studied via agarose gel precipitation experiments and the results were compared with available structural data.The LPS species could be divided into ConA-reactive and non-reactive ones. Reactivity resided in the O-specific chain of LPS, and binding to the lipid A or core moieties of LPS could not be demonstrated by the present methods.