ovalbumin and Pleural-Effusion

The interference of azelastine with pleurisy induced by antigen was investigated in actively sensitized rats. The antigenic challenge (ovalbumin, 12 micrograms/cavity) caused early plasma leakage, which peaked within 4 h, accompanied by intense neutrophil infiltration. Pleural exudate decayed 24 h after antigen provocation, when a long-lasting increase in the number of resident eosinophils was observed. Oral pretreatment with azelastine (1-10 mg/kg) dose dependently inhibited the vasopermeation (ED50 = 4.2 mg/kg) and reduced the pleural exudate (ED50 = 6.8 mg/kg) induced by the antigen. In contrast, azelastine (10 mg/kg) failed to modify the neutrophil influx observed at 4 h and the eosinophil accumulation detected at 24 h. Azelastine was also effective against rat pleurisy induced by either platelet-activating factor (PAF-acether), histamine or serotonin. It reduced exudation and the increase in the number of mononuclear cells, neutrophils and eosinophils observed 6 h after PAF-acether. Nevertheless, antagonism of PAF-acether may not be relevant to the inhibition observed in the present model of allergic pleurisy, as the inhibition was refractory to three distinct PAF-acether receptor antagonists. In contrast, like azelastine, the histamine H1 receptor antagonist meclizine and the dual histamine and serotonin receptor antagonist cyproheptadine blocked antigen-induced exudation and failed to interfere with cell influx. We conclude that the anti-exudatory activity of oral azelastine on antigen-induced pleurisy is consistent with it exerting direct effects against vasoactive amines, but is not related to an effect against leucocyte infiltration nor to its ability to inhibit PAF-acether.

Topics: Animals; Antigens; Female; Histamine; Histamine H1 Antagonists; Leukocytes; Male; Ovalbumin; Phthalazines; Platelet Activating Factor; Pleural Effusion; Pleurisy; Rats; Rats, Inbred Strains; Serotonin

This study was undertaken to characterize the different phases of the allergic pleurisy induced by ovalbumin in actively sensitized rats. The reaction was triggered by the intrathoracic injection of ovalbumin (12 micrograms/cavity) into animals sensitized 14 days before. The challenge caused, at 30 min, a drastic mast cell degranulation and exudation which peaked within 4 h. At this time, an intense pleural leucocyte recruitment also occurred, accounted for by an increase in the mononuclear cell counts and by a predominant influx of neutrophils. After 24 h, the mast cell counts started to recover, accompanied by a long-lasting (96 h) accumulation of pleural eosinophils. Forty-eight hours later, the exudation and neutrophils were at basal levels, whereas mast cell counts increased progressively to reach control values at 120 h. This study describes the time course of the exudative and cellular alterations observed during pleural inflammation induced by low antigen concentrations.

Topics: Acute Disease; Aluminum Hydroxide; Animals; Female; Kinetics; Leukocytes; Male; Mast Cells; Ovalbumin; Pleural Effusion; Pleurisy; Rats; Rats, Inbred Strains

Brown Norway rats were immunized with trinitrophenylated ovalbumin (TNP-OVA). TNP-specific and total IgE in serum and in acid eluates of pleural and peritoneal mast cells were determined by radioimmunoassay. The IgE load of peritoneal mast cells was significantly higher than the IgE load of pleural mast cells. 8-9 days after immunization, the ratio specific/total IgE for cell-bound IgE was smaller than this ratio for free circulating IgE. The composition of IgE on mast cells that were isolated 8-9 days after immunization was better reflected by the composition of serum IgE on the day before isolation than by the composition of serum IgE at the time of isolation of the mast cells. Therefore, we conclude that (1) IgE on mast cells is not in rapid equilibrium with free circulating IgE, and (2) the composition of IgE on mast cells lags at least 1 day behind that of serum IgE.

Topics: Animals; Ascitic Fluid; Binding Sites, Antibody; Epitopes; Immunoglobulin E; Mast Cells; Ovalbumin; Pleural Effusion; Rats; Rats, Inbred BN; Trinitrobenzenes

Studies have been made of movement of various macromolecules into and out of the pleural space of guinea pigs during the course of a delayed hypersensitivity reaction to purified protein derivative (PPD), and a passively transferred immediate hypersensitivity reaction to ovalbumin. While the immediate hypersensitivity reaction transiently alters vascular permeability as shown by increased movement of macromolecules into the chest, the delayed hypersensitivity reaction is marked by a decreased capacity to resorb macromolecules from the pleural space. The data suggest that the two hypersensitivity reactions may be distinguished by these physiologic differences. Additional data from studies of a chemically induced pleural effusion in these animals suggest that some type of outflow obstruction is necessary for the development of effusion, but that the outflow defect caused by the irritating chemical is based on a different mechanism than that seen during the delayed hypersensitivity reaction.

Topics: Animals; Biological Products; gamma-Globulins; Guinea Pigs; Hypersensitivity, Delayed; Hypersensitivity, Immediate; Immune Sera; Iodine Isotopes; Ovalbumin; Pleural Effusion; Pleurisy; Turpentine