IgG2 antibodies block IgE antibody-induced asthma in guinea pigs

In order to examine the blocking activity of IgG2 antibodies to guinea pig for IgE antibodies-induced guinea pig asthma, experiments were carried out as follows. Guinea pigs were passively sensitized intravenously with guinea pig serum containing IgE antibodies to ovalbumin (OA). 8 days after sensitization, IgG2 purified from guinea pigs hyperimmunized with OA was intravenously injected. One hour later, the guinea pigs were challenged by inhalation of OA solution. Asthma attacks were not observed in the guinea pigs, whereas the attacks were observed in guinea pigs passively sensitized with the IgE antibodies but injected IgG2 fraction from normal guinea pigs 1 h before inhalation. These observations suggested that IgG antibodies that increased after immunotherapy might block asthma caused by inhalation of allergens in humans.     

Enhancement of the in vitro antibody response in dietary protein restriction. Failure in the regulation of antibody synthesis.

We have studied the antibody response in vitro of spleen cells from C57BL/6 mice kept on a protein deficient (D) or a normal diet (N). Short or long term protein restriction initiated after weaning led to increased plaque forming cell (PFC) responses to sheep red blood cells (SRBC), TNP-ficoll and TNP lipopolysaccharide. The influence of dietary restriction on the suppression of the antibody response to SRBC was studied in mixed cultures of antigen sensitized and fresh, non-immune cells from either D or N donors. Addition of pre-sensitized D or N cells to non-immune N spleen cells in a 1:1000 ratio resulted in marked suppression of the PFC response whereas co-cultures of pre-sensitized cells and non-immune D spleen cells did not result in significant suppression. Similarly, non-immune T cells from DF mice exerted a lower suppressor effect than non-immune T cells from N mice. Either dietary restriction or low dose cyclophosphamide treatment of the donors of non-immune spleen cells determined a similar reduction in suppression. It is suggested that nutritional deficiency selectively depletes short-lived suppressor effector lymphocytes which are activated in the presence of antigen-stimulated inducer cells.     

Macrophage-activating T-cell factor(s) produced in an early phase of Legionella pneumophila infection in guinea pigs.

Protective immunity of guinea pigs against Legionella pneumophila was studied by infecting the animals with a sublethal dose (about 2 x 10(4) CFU) of the organism. The bacteria multiplied in the liver, spleen, and lungs up to day 4 after the intraperitoneal infection. The live bacteria in these organs decreased quickly thereafter and were eliminated by day 7. A delayed-type skin reaction and lymphoproliferation of spleen cells to Formalin-killed L. pneumophila were detected from days 5 and 6, respectively, after infection. Peritoneal macrophages obtained from guinea pigs infected 6 days previously inhibited the intracellular growth of L. pneumophila. Antigen-stimulated spleen cell factor prepared from infected guinea pigs inhibited the intracellular growth of the organism in macrophages obtained from uninfected animals. Antigen-stimulated spleen cell factor prepared from spleen cells treated with anti-guinea pig T-cell monoclonal antibody did not inhibit growth. The activity of antigen-stimulated spleen cell factor was labile to pH 2 treatment, and the factor could not be absorbed by L. pneumophila antigen, suggesting that it contains gamma interferon. Our data show that T-cell-mediated immunity begins to work from an early period of infection with L. pneumophila in guinea pigs.     

Suppression of reaginic antibody formation in guinea pigs by anti-idiotypic antibodies

Syngeneic immunization of strain 2 and strain 13 guinea pigs with purified antibodies against benzyl-penicilloyl bovine IgG (BPO-BGG) produces anti-idiotypic antibodies which specifically inhibit antigen-induced T cell proliferation in vitro. In sensitized guinea pigs, passive administration (either intravenously or subcutaneously in complete Freund's adjuvant [CFA] of these anti-idiotypic antibodies has a reversible suppressive effect on IgG and IgM responses. In addition, preimmunization with idiotypes effects a long-term and specific suppression of the production of homocytotropic antibodies against a hapten-protein conjugate (BPO-BGG). The suppression of the homocytotropic antibody response in already sensitized outbred guinea pigs was attempted by immunization with autologous serum, autologous antibodies, or autologous lymphoid cells. With all immunization procedures used so far, no significant suppressive effects could be demonstrated. The significance of these findings, in terms of the practical potential of autoanti-idiotypic immunization for the management of allergic diseases, is briefly discussed.     

Interactions Between Salmonellae and Macrophages of Guinea Pigs IV. Relationship Between Migration Inhibition and Antibacterial Action of Macrophages

The in vitro macrophage migration inhibition test was used to detect the development of delayed-type hypersensitivity in guinea pigs infected with Salmonella typhimurium. Four different preparations from supernatants of S. typhimurium cultures were used as the antigens in this test. They included the concentrated bacterial antigens, the high-molecular-weight (>50,000) antigens, the ammonium sulfate-precipitated antigens, and the ribonuclease-treated antigens. All four antigen preparations were shown to inhibit the migration of peritoneal macrophages of salmonella-infected (immune) guinea pigs from capillary tubes, in comparison with cells of normal control animals. By use of the high-molecular-weight antigens and the ammonium sulfate-precipitated antigens, the production of the migration inhibition factor(s) was elicited from cultures of lymphocytes obtained from the peripheral blood of immune guinea pigs. The activity of the migration inhibition factor(s) was demonstrated by its ability to inhibit the migration of peritoneal macrophages of normal guinea pigs from capillary tubes. In contrast, normal peritoneal macrophages exposed to products of antigen-stimulated immune lymphocytes did not exhibit an enhanced phagocytic or bactericidal action against virulent S. typhimurium as compared with those of the normal control. The present study indicated that the bacterial antigens responsible for the elicitation of the production of the migration inhibition factor from lymphocytes of immune guinea pigs are inactivated by proteolytic enzymes, but not by ribonuclease, and have molecular weights of >50,000.     

Isolation, characterization, and biological properties of a tuberculin-active peptidoglycan isolated from the culture filtrate of Mycobacterium tuberculosis.

A water-soluble tuberculin-active peptidoglycan (TAPG) with a molecular weight of ca. 28,000 to 30,000 was isolated from the culture filtrate of Mycobacterium tuberculosis. TAPG was approximately four to five times more potent than tuberculin purified protein derivative S in guinea pigs sensitized with M. tuberculosis or M. bovis (freeze-dried BCG). It showed little or no cross-reactivity at a dose of 0.1 to 0.4 microgram in guinea pigs sensitized with M. kansasii, M. scrofulaceum, M. intracellulare, or M. avium. TAPG did not show any adjuvant activity when injected in guinea pigs in a water-in-oil emulsion containing ovalbumin. TAPG, in Freund incomplete adjuvant, proved to be an effective immunogen for inducing delayed hypersensitivity in guinea pigs. Chemical analysis of TAPG showed that it contains proline, glutamic acid, alanine, diaminopimelic acid, tyrosine, threonine, glucosamine, and the reducing sugars, arabinose and galactose. In immunoelectrophoretic studies with reference M. tuberculosis H37Rv antiserum, TAPG did not show any precipitin bands.     

Antiallergic effect of epinastine (WAL 801 CL) on immediate hypersensitivity reactions: (I). Elucidation of the mechanism for histamine release inhibition.

Epinastine caused an inhibition of histamine release from rat peritoneal mast cells induced by both antigen-antibody reaction and compound 48/80. Epinastine was similarly effective in inhibiting compound 48/80-induced histamine release not only from isolated rat peritoneal mast cells but also from rat mesenterial pieces. Also, histamine release from lung pieces obtained from actively sensitized guinea pigs after exposure to antigen challenge was markedly inhibited by epinastine. The drug was effective in inhibiting not only Ca2+ uptake into lung mast cells in actively sensitized guinea pigs but also Ca2+ release from the intracellular Ca store of rat peritoneal mast cells exposed to both compound 48/80 and substance P. No significant changes were observed in phosphodiesterase activity in rat peritoneal mast cells treated with epinastine, while adenylate cyclase activity was augmented by epinastine. Epinastine has no inhibitory effect on histamine release induced by Ca2+ or IP3 from permeabilized mast cells. However, the drug significantly and dose-dependently suppressed calmodulin activity suggesting that histamine release inhibition due to epinastine may be partly attributable to Ca(2+)-calmodulin dependent process(es). The drug caused no visible changes in thermodynamic behavior of lipids, either in order parameter or in differential scanning calorimetry, indicating that the drug has no influence on membrane fluidity.     

Antiallergic Effect of Epinastine (WAL 801 CL) on Immediate Hypersensitivity Reactions: (I) Elucidation of the Mechanism for Histamine Release Inhibition

Epinastine caused an inhibition of histamine release from rat peritoneal mast cells induced by both antigen-antibody reaction and compound 48/80. Epinastine was similarly effective in inhibiting compound 48/80-induced histamine release not only from isolated rat peritoneal mast cells but also from rat mesenterial pieces. Also, histamine release from lung pieces obtained from actively sensitized guinea pigs after exposure to antigen challenge was markedly inhibited by epinastine. The drug was effective in inhibiting not only Ca²⁺ uptake into lung mast cells in actively sensitized guinea pigs but also Ca²⁺ release from the intracellular Ca store of rat peritoneal mast cells exposed to both compound 48/80 and substance P. No significant changes were observed in phosphodiesterase activity in rat peritoneal mast cells treated with epinastine, while adenylate cyclase activity was augmented by epinastine. Epinastine has no inhibitory effect on histamine release induced by Ca²⁺ or IP3 from permeabilized mast cells. However, the drug significantly and dose-dependently suppressed calmodulin activity suggesting that histamine release inhibition due to epinastine may be partly attributable to Ca²⁺-calmodulin dependent process(es). The drug caused no visible changes in thermodynamic behavior of lipids, either in order parameter or in differential scanning calorimetry, indicating that the drug has no influence on membrane fluidity.     

Elicitation of homologous passive cutaneous anaphylactic reactions by a benzylpenicillin preparation

Four out of five commercially available benzylpenicillin preparations elicited homologous passive cutaneous anaphylactic (PCA) reaction in sensitized guinea pigs with anti-benzylpenicilloyl (anti-BPO) reaginic sera. The same preparations could not evoke PCA reaction in sensitized guinea pigs with anti-BPO γ₁ homocytotropic antibodies. The PCA reactions were completely inhibited by a prior injection of BPO--aminocaproic acid (BPO-EACA). Chromatographic analysis of one of the benzylpenicillin preparations on Sephadex G 10 revealed that the reagin-mediated PCA reaction was not evoked with the fractions from the main peak of the benzylpenicillin but with fractions eluted earlier. None of the fractions gave positive γ₁-mediated PCA reactions. These results indicated that some commercial benzylpenicillin preparations contained minute amounts of the impurities that could elicit the homologous PCA reaction in guinea pigs sensitized with anti-BPO reaginic sera. It was also indicated that the PCA elicitation activity of the benzylpenicillin preparation in the system of reagin-mediated PCA differed from that of γ₁-mediated PCA.     

Airway eosinophils from actively sensitized guinea pigs exhibit enhanced superoxide anion release in response to antigen challenge.

Antigen challenge of actively sensitized guinea pigs produces airway eosinophilia, airway hyperreactivity, and late-phase bronchoconstriction. The recruited eosinophils are thought to be important cells in the development of the airway hyperreactivity and the late-phase bronchoconstriction. However, the functional abilities of these eosinophils have not been determined in response to antigen challenge. The purpose of this study was to describe the characteristics of superoxide anion release from airway eosinophils obtained 24 h after ovalbumin challenge of actively sensitized guinea pigs. Eosinophils were collected by bronchoalveolar lavage. The total bronchoalveolar lavage eosinophil count was 17- to 27-fold greater in sensitized, ovalbumin-challenged guinea pigs (9.30 +/- 0.11 x 10(6)/guinea pig) than in unsensitized guinea pigs (0.35 +/- 0.07 x 10(6)/guinea pig) or sensitized, saline-challenged guinea pigs (0.56 x 10(6)/guinea pig; n = 2). The increase in eosinophils was due to increased lavage leukocyte count and increased eosinophil differential. Eosinophils were isolated on a Percoll-plasma discontinuous gradient. Two populations of eosinophils were collected, one at the 1.093 g/ml gradient step and one at the 1.107 g/ml gradient step. Unstimulated or phorbol myristate acetate (PMA)-stimulated superoxide anion release was measured by the reduction of ferricytochrome c. Unstimulated superoxide anion release from both eosinophil populations of challenged guinea pigs (4.50 +/- 2.37 and 4.07 +/- 1.48 nmol from 1.093 and 1.107 g/ml eosinophils, respectively) was 6- to 7-fold greater than superoxide anion release from eosinophils of control guinea pigs (0.74 +/- 0.43 and 0.56 +/- 025 nmol from 1.093 and 1.107 g/ml eosinophils, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Characterization of increased cough sensitivity after antigen challenge in guinea pigs

Increased sensitivity of cough reflex is a fundamental feature of bronchodilator resistant non-productive cough associated with eosinophilic tracheobronchitis. Our hypothesis is that cough sensitivity is increased by airway allergic reaction characterized by airway eosinophilic inflammation. The aim of this study was to elucidate the hypothesis and clarify the characteristics of the increased cough sensitivity. Number of coughs elicited by inhalation of increasing concentrations of capsaicin (10-8, 10-6 and 10-4 M) was counted 24 h after an aerosolized antigen or saline in actively sensitized or non-sensitized (naive) conscious guinea pigs and then bronchoalveolar lavage was performed. The cough response was also measured 1 day before and 1, 2, 3, 5 and 7 days after an aerosolized antigen challenge in sensitized or naive animals. In addition, effect of procaterol (0.1 mg/kg), atropine (1 or 10 mg/kg), phosphoramidon (2.5 mg/kg) given intraperitoneally 30 min before the capsaicin challenge or capsaicin desensitization on the cough response was examined. Furthermore, the thromboxane A2 (TXA2) receptor antagonist S-1452 in a dose of 0.01 or 0.1 mg/kg or vehicle (saline) was given intraperitoneally at 24 and 1 h before the measurement of cough response. Number of coughs caused by capsaicin was extremely increased 24 h after an antigen challenge in sensitized guinea pigs compared with a saline or an antigen challenge in naive animals or a saline challenge in sensitized animals. The increased cough response disappeared at 3-7 days after the antigen challenge. Eosinophils in bronchoalveolar lavage fluid obtained after the measurement of capsaicin-induced coughs, which was performed 24 h after the antigen challenge, were significantly increased in sensitized guinea pigs. The eosinophil count was significantly correlated to the number of capsaicin-induced coughs. Procaterol or atropine did not alter the antigen-induced increase of cough sensitivity, whereas atropine did reduce the cough response in naive animals. Phosphoramidon increased the number of capsaicin-induced coughs in naive guinea pigs but not in sensitized and antigen-challenged animals. Capsaicin desensitization decreased the cough response in both antigen-challenged sensitized guinea pigs and naive animals. S-1452 reduced the antigen-induced increase of cough response in sensitized guinea pigs, but not in naive animals. Airway allergy accompanied with airway eosinophilia induces transient increase in cough sensitivity, which is not mediated by bronchoconstriction. The increased cough sensitivity may result in part from inactivation of neutral endopeptidase and TXA2, one of the inflammatory mediators.     

Anti-inflammatory actions of interleukin-13: suppression of tumor necrosis factor-alpha and antigen-induced leukocyte accumulation in the guinea pig lung

The Th2 cytokine interleukin (IL)-13 is believed to play an important role in the development of allergy, although it has also been ascribed anti-inflammatory roles in several experimental models. In this study, we have examined the effects of human recombinant IL-13 on eosinophilic lung inflammation in the guinea pig. IL-13 (1 to 100 ng, given by intratracheal instillation) did not elicit airway eosinophil recruitment. A pronounced accumulation of eosinophils, as well as monocyte/macrophages, was elicited by intratracheal instillation of guinea pig tumor necrosis factor alpha (gpTNF-alpha). Intratracheal administration of IL-13 (1 to 100 ng) given immediately prior to exposure to gpTNF-alpha resulted in a dose-related suppression of eosinophil and monocyte/macrophage accumulation in the airways, as assessed by bronchoalveolar lavage (BAL) and eosinophil peroxidase activity in whole-lung homogenates. IL-13 treatment also reduced BAL fluid (BALF) leukocyte accumulation induced by subsequent aerosol antigen challenge of sensitized guinea pigs. Antigen challenge also resulted in elevated levels of immunoreactive eotaxin and eosinophil-stimulating activity in BALF, although only the latter was reduced significantly by IL-13 instillation prior to challenge. In contrast to the suppressive effects of IL-13, instillation of human recombinant IL-4 (100 ng) alone elicited an increase in BALF monocyte/macrophage numbers, and IL-4 was unable to inhibit gpTNF-alpha-induced leukocyte accumulation. Hence, IL-13 (but not human IL-4) exhibits an anti-inflammatory action in the airways of gpTNF-alpha- or antigen-challenged guinea pigs, by mechanisms that may involve the decreased generation of eosinophil-stimulating activity in the airways.     

Antiallergic Effect of Epinastine (WAL 801 CL) on Immediate Hypersensitivity Reactions: (I) Elucidation of the Mechanism for Histamine Release Inhibition

Abstract

Epinastine caused an inhibition of histamine release from rat peritoneal mast cells induced by both antigen-antibody reaction and compound 48/80. Epinastine was similarly effective in inhibiting compound 48/80-induced histamine release not only from isolated rat peritoneal mast cells but also from rat mesenterial pieces. Also, histamine release from lung pieces obtained from actively sensitized guinea pigs after exposure to antigen challenge was markedly inhibited by epinastine. The drug was effective in inhibiting not only Ca²⁺ uptake into lung mast cells in actively sensitized guinea pigs but also Ca²⁺ release from the intracellular Ca store of rat peritoneal mast cells exposed to both compound 48/80 and substance P. No significant changes were observed in phosphodiesterase activity in rat peritoneal mast cells treated with epinastine, while adenylate cyclase activity was augmented by epinastine. Epinastine has no inhibitory effect on histamine release induced by Ca²⁺ or IP3 from permeabilized mast cells. However, the drug significantly and dose-dependently suppressed calmodulin activity suggesting that histamine release inhibition due to epinastine may be partly attributable to Ca²⁺-calmodulin dependent process(es). The drug caused no visible changes in thermodynamic behavior of lipids, either in order parameter or in differential scanning calorimetry, indicating that the drug has no influence on membrane fluidity.     

Immunohistochemical Localization of Secretory Component in the Liver of Guinea Pigs and Dogs versus Rats, Rabbits, and Mice

Secretory component (SC) was localized in the liver of guinea pigs, dogs, rabbits, rats, and mice. In rabbits, rats, and mice SC localized predominantly in bile canaliculi and on hepatocyte sinusoidal membranes but was doubtful in cholangincytes. In dogs and guinea pigs SC-staining was not detected in/on hepatocytes and canaliculi but was strong in/on cholangiocytes, as reported for humans. In guinea pigs IgA biliary output was small (0.23 mg/kg/day), as for dogs and humans, and below IgG output (1.4mg). in contrast to rats, whose IgA biliary output (38 mg/kg/day) was much larger than IgG output (2 mg). Biliary obstruction in guinea pigs induced only minor increases in serum IgA (+ 26% over 24 h), as reported for dogs and humans, in contrast to rats (+ 800% over 24 h) and rabbits. Hepatocyte SC expression correlates with IgA hepatobiliary excretion, being low in guinea pigs, dogs, and humans but high in rats, rabbits, and mice.     

气道速激肽在卵蛋白致敏豚鼠模型咳嗽反应中的作用

目的：研究气道速激肽在卵蛋白致敏和激发豚鼠咳嗽发生机制中的作用。 方法： 正常和卵蛋白致敏豚鼠各20只，卵蛋白雾化吸入激发。24 h后，正常组和致敏组豚鼠随机各分为2组，每组10只，分别依次腹腔注射生理盐水，0.1 mg/kg、0.3 mg/kg和1.0 mg/kg的NK1受体拮抗剂SR140333 或NK2受体拮抗剂SR48968，观察吸入10-4 mol/L的辣椒素溶液诱导的咳嗽反应。用非侵入性方法测量正常和卵蛋白致敏豚鼠注射SR140333或SR48968前后吸入辣椒素溶液所产生的特异性气道阻力。 结果： 致敏豚鼠咳嗽反应明显高于正常对照组［(9.3±1.2)times/3 min vs (19.5±5.7)times/3 min，P<0.05］。SR140333不影响正常对照组豚鼠的咳嗽反应，而SR48968则可降低咳嗽频率达30% (P<0.05)，两者均抑制吸入辣椒素后增加的气道阻力。而在卵蛋白致敏豚鼠，SR140333或SR48968均抑制吸入辣椒素溶液诱导的咳嗽频率［(9.9±4.7)times/3 min，(8.0±1.6)times/3 min，P<0.05］和增高的气道阻力。 结论： NK受体拮抗剂抑制致敏豚鼠卵蛋白激发后增高的咳嗽反应。因此，气道速激肽可能是嗜酸性粒细胞性气道炎症所致咳嗽的重要介质。     

Immunologic Events in Experimental Hypersensitivity Granulomas

Polyacrylamide beads were covalently linked to proteins and injected intravenously into normal or immune guinea pigs. The beads trapped in the lung produced very mild foreign body granulomas in nonimmune guinea pigs. In immune guinea pigs, severe granulomas developed which progressed through the several characteristic histologic stages with time. Severe granulomatous reactions developed only upon recognition of carrier determinants of hapten-protein conjugates; thus guinea pigs immune to dinitrophenyl hapten (DNP)-hemocyanin developed characteristic granulomas only upon injection of beads coated with hemocyanin or DNP-hemocyanin, but not with DNP on another unrelated antigen. Granulomatous reactivity was passively transferred into normal animals by lymph node cells but not by serum antibody from sensitized guinea pigs.     

Bronchial hyperresponsiveness to histamine following antigen challenges in actively sensitized guinea pigs

Guinea pigs were actively sensitized by intraperitoneally administered ovalbumin and challenged by intravenous injections of ovalbumin. Respiratory resistance and dynamic compliance were measured by pulmonary mechanics analyzer Buxco Model 6. Changes in resistance (delta R) and compliance (delta C) induced by intravenously administered histamine were investigated before and after the challenge. Responses to the histamine in sensitized guinea pigs were also compared with those in naive guinea pigs. The following results were obtained. 1) A significant increase in delta R by histamine administration was observed following the antigen challenge. delta C by histamine administration showed a tendency to increase after the challenge. 2) A significant increase of delta R by 7.2 micrograms/kg histamine administration was observed in actively sensitized guinea pigs. However, delta C by the histamine administration did not change in the sensitized animals.     

Specific immunological and bronchopulmonary responses following intradermal sensitization to free trimellitic anhydride in guinea pigs

We have developed a guinea pig model of trimellitic anhydride-induced airway hypersensitivity responses. In one group of guinea pigs, injected intradermally with 0.1 ml 30% trimellitic anhydride (TMA), we examined the specificity of the bronchopulmonary response to TMA comparing the effect of intravenous TMA conjugated to guinea pig serum albumin (GPSA) with a control hapten (procion dye) protein conjugate (PD-GPSA). A significant increase in pulmonary inflation pressure (PIP) was provoked in sensitized animals following intravenous injection with TMA-GPSA (20%; 0-400, median; range) as compared to intravenous injection of PD-GPSA. In the second group we compared three different methods of sensitization: single injection of 0.1 ml of 0.3% TMA; four injections of 0.1 ml of 0.1% TMA; and a single high dose injection of 30% TMA. Following intravenous TMA-GPSA guinea pigs sensitized with a single injection 0.3% TMA had an increase in PIP of 395%; 220-600, while those given four repeat injections of 0.1% TMA had an increase in PIP of 343%; 315-490. These results were significantly higher than the increase in PIP (160%; 0-220) which occurred in guinea pigs sensitized with a single dose of 30% TMA. Four of 11 guinea pigs given low dose injections of TMA had bronchopulmonary responses to inhaled TMA-GPSA. All sensitized guinea pigs had specific IgG1 antibodies demonstrated by enzyme linked immunosorbent assay (ELISA) and confirmed by ELISA inhibition. Four guinea pigs sensitized by low dose injections of TMA had IgE antibodies demonstrated by passive cutaneous anaphylaxis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cellular Immunity In Vitro: Migration Inhibition and Phagocytosis

The activity of peritoneal exudate cells from candidin-sensitive and normal guinea pigs with and without antigen was studied in vitro with the aid of time-lapse, phase-contrast cinemicrography. Macrophages from normal animals migrate well on an agar medium and readily phagocytose Merthiolate-killed Candida albicans cells. A reduction in the migration of peritoneal macrophages from guinea pigs sensitized to C. albicans during the first 24 hr after exposure to antigen was accompanied by a decrease in phagocytosis of C. albicans cells. The macrophages were viable but comparatively immotile. Since the sensitized macrophages came from resistant donors, it is possible that the initial stage of cellular immunity to C. albicans is associated with a reduced activity of the phagocytic macrophages, apparently to limit spread of the pathogen from the infected area.     

Inhibition of allergen-induced bronchoconstriction in sensitized guinea pigs by orally administered allergen

Crude mite extract (CME) was orally administered to guinea pigs sensitized to CME. It was shown that such treatment reduces the bronchoconstrictive response upon allergen provocation. Isolated tracheae taken from guinea pigs orally administered CME allergen showed less contraction in response to CME as compared to those obtained from sensitized but not orally treated animals. The oral administration of allergens seemed to attenuate the bronchial hyperresponsiveness of sensitized animals to a non-specific chemical stimulus (histamine). IgE antibodies titrated by 8 days passive cutaneous anaphylaxis, and IgG1 and IgG2 antibodies measured by ELISA were comparable in the sera obtained from animals before and after CME treatment.