International archives of allergy and applied immunology最新文献

Recently, we demonstrated that lipopolysaccharide (LPS)-hyporesponsive C3H/HeJ mice show a very high background number of splenic antibody-forming cells with specificity for bromelain-treated isologous erythrocytes. This background level was not or only slightly enhanced by LPS injection. In this paper it is reported that the existing response of C3H/HeJ mice is about doubled by treatment of the animals with cobra venom factor (CVF). This increase is very similar to the LPS-induced potentiation of the auto-antibody response of C3H/Tif and other LPS-responder mice. The absence of auto-antibodies in the sera of CVF-treated C3H/HeJ mice, however, points at a different mechanism of B cell activation. The mediation of the CVF-induced stimulation of the B cells of C3H/HeJ mice by covalent C3-glycoprotein complexes and the need for an additional stimulus is discussed.

The possible regulatory role of beta 2-adrenoceptor agonists in the modulation of CD23 on the human promonocytic cell line U937 and on human monocytes was investigated. Incubation for 48 h in the presence of interleukin-4 (IL-4; 30 U/ml) induced optimal expression and release of CD23 on both U937 cells and human monocytes. When a beta 2-adrenoceptor agonist, either salbutamol or fenoterol, was added to U937 cells or monocytes both the IL-4-induced CD23 expression and release were markedly up-regulated. This effect was dose-dependent, starting at 10 nM and reaching a maximum at 1 microM final concentration of either salbutamol or fenoterol. The potentiating effect of salbutamol and fenoterol on CD23 expression and release was not observed when a beta-adrenoceptor antagonist, either D,L-propranolol (1 microM) or butoxamine (1 microM), was added to the incubation medium. The alpha-adrenoceptor agonist norepinephrine (1 microM) was ineffective in enhancing the IL-4-induced expression and release of CD23 from U937 cells or human monocytes, demonstrating the specificity of the beta 2-adrenoceptor-mediated effect. In the absence of IL-4, a moderate but significant increase in the CD23 expression on U937 cells and human monocytes by these drugs was observed, as compared to the basal values. These results indicate that, besides their bronchodilator effect, beta 2-adrenoceptor agonists may regulate IgE-dependent processes.

Lysophosphatidylserine (lysoPS) is known to enhance IgE-mediated activation of rodent connective tissue mast cells (CTMCs). In the present study, we investigated the effect of lysoPS on degranulation of interleukin-3-dependent mouse bone marrow-derived mucosal mast cells (BMMCs) and of their CTMC-like differentiated cells. In the absence of lysoPS, BMMCs released approximately 20% of their histamine when sensitized with anti-dinitrophenyl (DNP) IgE and challenged with DNP-conjugated antigen. When stimulated in the presence of lysoPS, no appreciable enhancement was observed. On the other hand, histamine release from BMMCs, which had differentiated to CTMC-like cells by co-culture with 3T3 fibroblasts, was enhanced 2- to 3-fold by the addition of lysoPS. The maximum potentiation was observed at 5 x 10(-6) M lysoPS. These results suggest that mast cells might acquire their dependence on exogenous lysoPS during differentiation from mucosal mast cells to CTMC-like cells.

Phospholipase A2 (PLA2) from cobra (Naja naja) venom and PLA2 from porcine pancreas accelerated IgE antibody-mediated histamine release from rat peritoneal mast cells. These enhancements were clearly abrogated by heating the enzymes and pretreatment with parabromophenacyl bromide, mepacrine and antiflammin. Indomethacin (cyclooxygenase inhibitor) and AA-861 (lipoxygenase inhibitor) did not affect the enhancement by PLA2. These results indicate that extracellular PLA2 enhances the IgE antibody-mediated histamine release from rat peritoneal mast cells without the participation of arachidonate.

The enzyme amylase was shown to be present in extracts prepared from both house dust and spent growth medium used in the culture of the mite Dermatophagoides pteronyssinus. In dust, it was shown to correlate with both mite counts and concentrations of the faecally derived mite allergen, Der p I. Mite amylase was isolated from the culture medium and shown to be a single chain protein with a molecular weight of 56,000. The enzyme contained free sulphydryl groups and had the N-terminal sequence, KYXNPHFIGXRSVITXLME. It was found to be an allergen using sera from adults (46% positive) and children (25%) who were mite allergic. The expression of allergenicity was dependent on the integrity of intra-chain disulphide bonds.

In this work we studied the IgG isotypes induced in mice immunized with two Trypanosoma cruzi acidic antigenic fractions (F IV and Eas 4.5) and the level of protection to a later infection with parasites. F IV is a cytosolic antigen from epimastigotes, and Eas 4.5 is an exoantigen released by trypomastigotes. The most relevant epitopes of Eas 4.5 are carbohydrates. A high prevalence of IgG1, low levels of IgG3 and no IgG2 antibodies against F IV and Eas 4.5 were found in sera obtained 2 weeks after the last antigen dose from animals immunized with F IV (group I) or Eas 4.5 (group II). Immunized mice from both groups were infected with trypomastigotes, and the parasitemias detected later on were significantly lower than in control groups (p less than 0.01, group I; p less than 0.001, group II). The amount of IgG2-specific antibodies, which was only detected using epimastigotes as antigen in ELISA, was significantly increased after the infection, but no major changes were seen in the profiles of other isotypes.

An attack of experimental allergic encephalomyelitis is generally thought to confer resistance to a second attack. Nevertheless, some authors have produced second attacks, sometimes with an anamnestic shortening of the incubation period. In addition, second attacks of experimental allergic encephalomyelitis with accelerated onsets following reinoculation were found in every experiment when histopathologic rather than clinical criteria were employed. In the present work, we found that clinical signs with accelerated onset were also found in each experiment provided that the first attack was produced with the aid of Freund's complete adjuvant and provided that the reinoculation stimulus was the highly potent combination of rat spinal cord and carbonyl iron. Whatever the potency of the reinoculation, and regardless of the occurrence of an accelerated onset, the eventual outcome was a decreased severity and mortality of the second attack of experimental allergic encephalomyelitis. The new data demonstrate that accelerated onset is not necessarily an indication of increased severity.

The allergenic components of water-soluble rye flour extract were studied by immunoblotting. Sera from 100 bakers were analyzed for their IgG, IgG4 and IgE binding pattern. Two allergens with molecular weights of 35 and 14 kD were detected. Previously, the major allergens of wheat flour extract were identified. The wheat flour components at a MW of 15/17 kD and the rye flour component at a MW of 14 kD were purified and isolated. The modulation of the low affinity receptor for IgE (Fc epsilon RII/CD23) on monocytes by separated allergenic components was studied. Depending on the allergen concentration the CD23 expression on isolated cells increased after stimulation with the rye flour component (MW 14 kD). The combined addition of the rye flour component (14 kD) with IL-4 induced a significant CD23 expression as compared to IL-4 alone.

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.