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Los mastocitos son células que participan en actividades de hipersensibilidad inmediata y tardía, inmunorregulación e inflamación. Recientemente se han detectado dos grupos de ellos: a) los que se localizan en tejido conjuntivo y b) los de la mucosa intestinal. Entre ellos hay diferencias morfológicas y funcionales. Los de mucosa intestinal son T dependientes y proliferan durante las parasitosis así como en los procesos de hipersensibilidad intestinal a diversos antígenos. Las placas de Peyer (PP) son los sitios principales donde se captan antígenos e inician las respuestas inmunitarias en el intestino, por lo que en este trabajo investigamos la relación morfológica entre las células de las PP y los mastocitos. Las PP de segmentos proximal, medial y distal del intestino delgado de ratones Balb/c se procesaron histológicamente, tiñeron con azul de toluidina y cuantificaron los mastocitos en las diferentes capas del intestino. Los datos se analizaron mediante una prueba de doble T pareada para diferencia de medios. Se observó mayor cantidad de mastocitos en la zona marginal de la PP en comparación con las capas: muscular resistente, submucosa y corion. La abundancia de mastocitos en relación con la PP sugiere que probablemente tenga influencia moduladora sobre la unción de las células linfoides de la PP

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This study was undertaken to characteize the different phases of the allergic pleurisy induced by ovalbumin in actively sinsitized rats. The reaction was triggered by the intrathoracic injection of ovalbumin (12 microng/cavity) into animals sensitized 14 days before. The challenge caused, at 30 mjin, a drastic mast cell degranulation and exudation which peaked within 4h. At this time, an intense pleural leucocyte recruitment also occurred, accounted for by an increase in the mononuclear cell counts and by a predominant influyx of neutrophils. After 24h, the mast cell counts stated to reover, accompanied by a long-lasting (96 h) accumaltion of pleural eosinophils. Forty-eight hour 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 exudatory and cellular alterations observed during pleural inflammation induced by low antigen concentrations

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1. The consequences of acute Trypanosoma cruzi infection for acetylcholine and histamine levels in gastric wall and for mast cells of the stomach were studied in rats. 2. Intraperitoneal infection with 4,000 trypomastigotes/g of a Y strain of Trypanosoma cruzi led to a 4-fold decrease in gastric acetylcholine level and to a 57- and 15-fold increase in histamine content in the membranous and glandular regions of the rat stomach, respectively. 3. Infection of rats with Trypanosoma cruzi also induced a 2- and 4-fold increase in mast cell numbers in the membranous and glandular regions of the muscle layer of the gastric wall, respectively, and a ganglionic inflammatory reaction with predominance of mononuclear cells. 4. We conclude that in acutely Trypanosoma cruzi-infected rats, the reduction of acetylcholine content is due to gastric denervation and that the histamine increase might be secondary to gastric denervation and/or to an increase in the number of mast cells of the gastric wall.

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The ammoniacal silver method, which identifies basic proteins, gives a positive reaction in cytoplasmic granules of rat peritoneal mast cells. However, in cytoplasmic granules of mucosal mast cells in the small intestine of the rat, this reaction is negative.

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The consequences of acute Trypanosoma cruzi infection for acetylcholine and histamine levels in gastric wall and for mast cells of the stomach were studied in rats. Intraperitoneal infection with 4,000 trypomastigotes/g of a Y strain of Trypanosoma cruzi led to a 4-fold decrease in gastric acetylcholine level and to a 57 - and 15-fold increase in histamine content in the membranous and glandular regions of the rat stomach, respectively. Infection of rats with Trypanosoma cruzi also induced a 2- and 4-fold increase in mast cell numbers in the membranous and glandular regions of the muscle layer of the gastric wall, respectively, and a ganglionic inflammatory reaction with predominance of mononuclear cells. We conclude that in acutely Trypanosoma cruzi-infected rats, the reduction of acetylcholine content is due to gastric denervation and that the histamine increase might be secondary to gastric denervation and/or to an increase in the number of mast cells of the gastric wall

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En nuestro estudio previo sobre la naturaleza de las células que infiltran los tejidos cardíacos en la cardiopatía crónica chagásica severa, hallamos que muchas células cebadas (mastocitos están presentes en contacto con la superficie celular de fibras musculares cardíacas. El hallazgo fue realizado en 3 casos sobre 3 estudiados, mediante una técnica con Azul de toluidina para reconocer células cebadas. Los mastocitos son grandes productores y secretores de histamina. Esta última sustancia, la cual es secretada en el curso de reacciones inmunológicas, tiene efecto dromotrópico-negativo, es capaz de pertubar la conducción aurículo-ventricular curso de reacciones inmunológicas, tiene efecto fromotrópico-negativo, es capaz de perturbar la conducción aurículo-ventricular y, tmabién, de inducir arritmias ventriculares. Los desórdenes de la conducción y del ritmo cardíaco son manifestaciones promenientes de la cardiopatía chagásica. Por, todos esos aspectos, nosotros creemos que la presencia de mastocitos en contacto con miocitos cardíacos sugiere que los primeros pueden ser factor de disfuncionalismo cardíaco, y es en un tema que merece ulteriores estudios

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En nuestro estudio previo sobre la naturaleza de las células que infiltran los tejidos cardíacos en la cardiopatía crónica chagásica severa, hallamos que muchas células cebadas (mastocitos están presentes en contacto con la superficie celular de fibras musculares cardíacas. El hallazgo fue realizado en 3 casos sobre 3 estudiados, mediante una técnica con Azul de toluidina para reconocer células cebadas. Los mastocitos son grandes productores y secretores de histamina. Esta última sustancia, la cual es secretada en el curso de reacciones inmunológicas, tiene efecto dromotrópico-negativo, es capaz de pertubar la conducción aurículo-ventricular curso de reacciones inmunológicas, tiene efecto fromotrópico-negativo, es capaz de perturbar la conducción aurículo-ventricular y, tmabién, de inducir arritmias ventriculares. Los desórdenes de la conducción y del ritmo cardíaco son manifestaciones promenientes de la cardiopatía chagásica. Por, todos esos aspectos, nosotros creemos que la presencia de mastocitos en contacto con miocitos cardíacos sugiere que los primeros pueden ser factor de disfuncionalismo cardíaco, y es en un tema que merece ulteriores estudios (AU)

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Suspensions of enzymatically dispersed human lung parenchymal mast cells were fractionated according to density by flotation through discontinuous Percoll gradients and examined for their responsiveness to release stimulants and pharmacologic agonists. Mast cells localized to all six density fractions (I-VI) examined: densities varied from specific gravities of 1.053 gm/ml to 1.123 gm/ml. Most (67%) lung mast cells localized to fractions III and IV, corresponding to specific gravities of 1.077 to 1.088 gm/ml, respectively. Histamine content increased with density from 2.7 +/- 0.3 pg per cell in fraction 1 to 4.8 +/- 0.7 pg per cell in fraction VI (mean +/- SEM; n = 19). Fraction III was least responsive to high concentrations of anti-IgE than to any other fractions and, along with fraction IV, the most responsive to ionophore A23187. All fractions released the arachidonate mediators prostaglandin D2 and leukotriene C4 in response to anti-IgE. In four of eight lungs tested, formyl methionine peptide (10(-6) to 10(-4) mol/L) weakly elicited histamine release (3% to 6%) in fractions I and II cells. Compound 48/80 (0.1 to 10 micrograms/ml; n = 3) failed to induce histamine release in any fractions. The cyclic adenosine monophosphate-active drugs, isoproterenol (10(-4) mol/L), dibutyryl cyclic adenosine monophosphate (3 mmol/L), and isobutylmethylxanthine (3 X 10(-4) mol/L) inhibited anti-IgE-induced histamine release from all fractions equivalently. Dimaprit (3 X 10(-5) mol/L) and cromolyn sodium (10(-5) -3 x 10(-3) mol/L) failed to significantly inhibit any fraction.(ABSTRACT TRUNCATED AT 250 WORDS)

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Rats infected with the helminth Nippostrongylus brasiliensis were injected i.p. with 2 mCi of [35S] sulfate on days 13, 15, 17, and 19 after infection. The intestines were removed from animals on day 20 or 21 after infection, the intestinal cells were obtained by collagenase treatment and mechanical dispersion of the tissue, and the 35S-labeled mucosal mast cells (MMC) were enriched to 60 to 65% purity by Percoll centrifugation. The cell-associated 35S-labeled proteoglycans were extracted from the MMC-enriched cell preparation by the addition of detergent and 4 M guanidine HCl and were partially purified by density gradient centrifugation. The isolated proteoglycans were of approximately 150,000 m.w., were resistant to pronase degradation, and contained highly sulfated chondroitin sulfate side chains. Analysis by high-performance liquid chromatography of chondroitinase ABC-treated 35S-labeled proteoglycans from these rat MMC revealed that the chondroitin sulfate chains consisted predominantly of disaccharides with the disulfated di-B structure (IdUA-2SO4----GalNAc-4SO4) and disaccharides with the monosulfated A structure (G1cUA----GalNAc-4SO4). The ratio of disaccharides of the di-B to A structure ranged from 0.4 to 1.6 in three experiments. Small amounts of chondroitin sulfate E disaccharides (GlcUA----GalNAc-4,6-diSO4) were also detected in the chondroitinase ABC digests of the purified rat MMC proteoglycans, but no nitrous acid-susceptible heparin/heparan sulfate glycosaminoglycans were detected. The presence in normal mammalian cells of chondroitin sulfate proteoglycans that contain such a high percentage of the unusual disulfated di-B disaccharide has not been previously reported. The rat intestinal MMC proteoglycans are the first chondroitin sulfate proteoglycans that have been isolated from an enriched population of normal mast cells. They are homologous to the chondroitin sulfate-rich proteoglycans of the transformed rat basophilic leukemia-1 cell and the cultured interleukin 3-dependent mouse bone marrow-derived mast cell, in that these chondroitin sulfate proteoglycans as well as rat serosal mast cell heparin proteoglycans are all highly sulfated, protease-resistant proteoglycans.

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We have previously shown that mast cells with the morphological and biochemical properties of mucosal mast cells (MMC) proliferate and mature in rat bone marrow cultures stimulated with factors from antigen or mitogen-activated T lymphocytes. Here we have used this system to explore the MMC hyperplasia which occurs in infections with gastrointestinal nematode parasites. Lymphocytes producing MMC-growth factor were present from day 10 onwards in N. brasiliensis-infected rats and mesenteric lymph nodes (MLN) were the major source of activated lymphocytes. When different tissues of normal rats were cultured in the presence of conditioned medium by far the greatest proliferation of MMC occurred in bone marrow, indicating an origin of MMC from haemopoietic precursors. Cultures of infected rat bone marrow yielded considerably greater numbers of MMC than cultures of normal rat bone marrow and experiments using semisolid culture media indicated that N. brasiliensis infection causes an increase in the frequency of MMC progenitors in the bone marrow. A scheme is put forward for the sequence of events occurring in vivo based on the results of these and other published experiments. The reasons for the restricted in vivo localization of MMC to the mucous membranes and associated lymph nodes is discussed. Finally we give the results of microspectrophotometric analysis which has shown that the cultured mast cell contain a non-heparin proteoglycan, thus adding a further feature to the list of MMC-like properties of these cells.

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