RESUMEN
Immunoglobulin E (IgE) has been shown to play a critical role in the allergic late-phase reaction, which is marked by intense leukocyte infiltration and edema. In this study we assessed the allergic pleural inflammation triggered by intrapleural (i.pl.) challenge in sensitized rats. We examined pleural effluent from actively sensitized rats following anti-IgE monoclonal antibody (mAb) (MARE-1) provocation for protein exudation, neutrophil as well as eosinophil accumulation. Inflammatory changes triggered by antigen after passive sensitization with IgE mAb was also assessed for comparison. Total serum level of IgE was found to be about threefold increased 7-8 days post-active sensitization, remaining augmented for at least 30 days. Increased levels of peritoneal leukocyte-bound IgE and serum IgE with specificity to ovalbumin were also detected. Nevertheless, the anti-IgE challenge in 14-day actively sensitized was shown to be a weak stimulus of neutrophil and eosinophil accumulation, despite being able to cause intense protein extravasation. Similarly, antigen challenge of IgE-passively sensitized rats caused protein leakage that was comparable to that induced by anti-IgE mAb in actively sensitized rats but led to a much lower neutrophil/eosinophil infiltration. Also, blockade of complement with recombinant human soluble C receptor-1 (sCR1) treatment prevented actively sensitized rats from reacting to antigen with neutrophil and eosinophil recruitment without modifying protein extravasation. These data suggest that IgE and complement-mediated mechanisms probably account for the exudation and leukocyte infiltration that is characteristic of the pleural inflammatory response observed in actively sensitized rats.
Asunto(s)
Inmunoglobulina E/inmunología , Pleuresia/inmunología , Proteínas/inmunología , Cloruro de Aluminio , Compuestos de Aluminio , Animales , Anticuerpos Monoclonales/inmunología , Cloruros , Eosinófilos/efectos de los fármacos , Femenino , Inmunoglobulina E/sangre , Recuento de Leucocitos/efectos de los fármacos , Masculino , Neutrófilos/efectos de los fármacos , Ovalbúmina/inmunología , Proteínas/metabolismo , Ratas , Ratas Wistar , Receptores de Complemento/inmunologíaRESUMEN
The identity of the histamine-potentiating activity detected in the rat anaphylactic pleural washing was investigated. Wistar rats of both sexes, weighing 150-200 g, were sensitized by injecting subcutaneously (sc) a mixture of ovalbumin and Al(OH)3 14 days before allergen challenge. In sensitized rats, intrapleural (ipl) injection of ovalbumin (12 micrograms/cavity) caused an intense protein exudation. A single ipl administration of compound 48/80 (12 micrograms/cavity) exhausted the resident mast cell population and turned the pleural cavity hyporeactive to the allergen challenge performed 5 days later. Allergen-induced exudation occurred in parallel to a dramatic decrease in the amount of cell-stored histamine (from 9.6 +/- 1.4 (N = 8) to 1.3 +/- 0.1 (N = 6) micrograms/cavity, P < 0.001) in the pleural fluid within 10 min. The anaphylactic cell-free pleural washing obtained at this time, as well as histamine at a concentration equivalent to that stored in pleural mast cells (10 micrograms/cavity), did not induce pleural exudation when injected into normal rats. In contrast, the combined administration of histamine and anaphylactic pleural washing led to remarkable pleural exudation, comparable to that obtained with a high dose of histamine (200 micrograms/cavity) alone. It is noteworthy that the anaphylactic washing from compound 48/80-pretreated rats failed to synergize with histamine. Also, synergism was not reproduced when recipient rats were pretreated with methysergide (50 micrograms/cavity). Consistently, serotonin (5 micrograms/cavity) acted synergistically with histamine (10 micrograms/cavity), producing a greater exudative response than observed with the sum of the effects of each vasoactive amine alone. The results indicate that serotonin accounts for the histamine-potentiating activity noted in the anaphylactic pleural washing, confirming that the synergistic interaction between these vasoactive amines plays a critical role in the rat allergic pleurisy.
Asunto(s)
Histamina/inmunología , Derrame Pleural/inmunología , Serotonina/inmunología , Anafilaxia/inmunología , Animales , Femenino , Masculino , Pleura/inmunología , Derrame Pleural/patología , Ratas , Ratas WistarRESUMEN
The identity of the histamine-potentiating activity detected in the rat anaphylactic pleural washing was investigated. Wistar rats of both sexes, weighing 150-200 g, were sensitized by injecting subcutaneously (sc) a mixture of ovalbumin and Al(OH)3 14 days before allergen challenge. In sensitized rats, intrapleural (ipl) injection of ovalbumin (l2 mug/cavity) caused an intense protein exudation. A single ipl administration of compound 48/80 (l2 mug/cavity) exhausted the resident mast cell population and turned the pleural cavity hyporeactive to the allergen challenge performed 5 days later. Allergen-induced exudation occurred in parallel to a dramatic decrease in the amount of cell-stored histamine (from 9.6 ñ 1.4 (N = 8) to 1.3 ñ 0.1 (N = 6) mug/cavity, P<0.001) in the pleural fluid within 10 min. The anaphylactic cell-free pleural washing obtained at this time, as well as histamine at a concentration equivalent to that stored in pleural mast cells (10 mug/cavity), did not induce pleural exudation when injected into normal rats. In contrast the combined administration of histamine and anaphylactic pleural washing led to remarkable pleural exudation, comparable to that obtained with a high dose of histamine (200 mug/cavity) alone. It is noteworthy that the anaphylactic washing from compound 48/80 pretreated rats failed to synergize with histamine. Also, synergism was not reproduced when recipient rats were pretreated with methysergide (50 mug/cavity). Consistently, serotonin (5 mug/cavity) acted synergistically with histamine (1O mug/cavity), producing a greater exudative response than observed with the sum of the effects of each vasoactive amine alone. The results indicate that serotonin accounts for the histamine-potentiating activity noted in the anaphylactic pleural washing, confirming that the synergistic interaction between these vasoactive amines plays a critical role in the rat allergic pleurisy.
Asunto(s)
Ratas , Animales , Femenino , Anafilaxia/patología , Histamina/farmacología , Pleura/efectos de los fármacos , Serotonina/farmacología , Derrame Pleural/patología , Pleuresia , Ratas WistarRESUMEN
Since essential fatty acids are required for normal brain development, we studied plasma lipids and EFA levels in 16 postpartum mothers (28 to 44 weeks) and in the umbilical vein and artery of 32 newborn infants. Groups of eight 24 to 33-, 34 to 37-, 38 to 42-, and 43 to 44-week-old infants were studied. Plasma fatty acid composition was studied in PL, CE, TG, and FFA by thin-layer and gas-liquid chromatography. Increased values for PL, CE, and TG (P less than 0.001) were noted in maternal plasma compared to cord plasma; linoleic acid was lower (P less than 0.001) in cord plasma PL, CE, and FA. EFA derivatives dihomo-gamma-linolenic, arachidonic, and docosahexaenoic acids were higher in cord plasma (P less than 0.001). Total polyenoic EFA increased with advanced gestation, and at term, was close to maternal levels. delta-5,8,11-eicosatrienoic acid (elevated in EFA deficiency) was elevated in cord plasma as compared with maternal values (P less than 0.001); other criteria of EFA deficiency were absent. These data indicate that fetal EFAs are elongated and desaturated during the third trimester. These higher polyenoic acids may incorporate into lipids in the developing CNS. The lower linoleic acid levels in the fetus may be important to the transplacental transport of EFA.