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At least 37 records · Page 2Linked to original sources
PubMed1985

Iota-carrageenan induced reaginic antibody production in the rat--I. Characterisation and kinetics of the response.

The intraperitoneal injection of graded amounts of ovalbumin into inbred PVG strain rats was found to produce a dose dependent anti-ovalbumin antibody response without eliciting the production of ovalbumin-specific reaginic antibodies. The injection of ovalbumin admixed with iota-carrageenan enhanced the anti-ovalbumin response and simultaneously elicited the de novo production of reaginic anti-ovalbumin antibodies. Isotype analysis of the anti-sera revealed the presence of both IgG and IgE class anti-ovalbumin antibodies and demonstrated that non-reaginic IgE anti-ovalbumin antibodies were also a feature of this reaction. The reaginic antibody phase of the response, although transient in nature, was re-elicited by secondary antigen challenge. The administration of ovalbumin prior to the ovalbumin-carrageenan preparation was shown to abrogate the reaginic antibody response without significantly influencing the non-reaginic component of the response. Conversely the injection of iota-carrageenan prior to antigen, significantly suppressed the normal agglutinating anti-ovalbumin response but did not prevent the induction of reaginic antibodies. These observations demonstrate that iota-carrageenan can, under specific conditions, function as an efficient adjuvant, and is capable of by-passing the normal mechanisms responsible for controlling antigen specific reaginic antibody production.

Animals↗
PubMed1976

Studies on immune responses to parasite antigens in mice. II. Aspects of the T cell dependence of circulating reagin production to Ascaris suum antigens.

Heat-labile, rat skin-fixing antibodies were detected readily in the sera of young female mice dosed intranasally with the body fluid of Ascaris suum (ABF) and the adjuvant, Bordetella pertussis vaccine (BPV). In addition, washed cell suspensions prepared from spleen and the lymph nodes regional to the lungs were positive in an adoptive cutaneous anaphylaxis assay, an assay which may detect activities of reagins associated with mast cells rather than reaginic antibody-secreting cells. The intraperitoneal route was a poor means of inducing circulating anti-ABF reagins and an intraperitoneal injection of ABF + BPV delayed the appearance of circulating reagins in mice dosed at the same time with ABF + BPV intranasally. Hypothymic female BALB/c. nu/nu ('nude') mice failed to produce circulating reagins to ABF but an injection of normal thymocytes or cortisone-resistant thymocytes from syngeneic female mice led to higher titers of circulating reagins than found in normal female BALB/c. nu/+ littermates. Using cells from young male or female syngeneic donors and male and female BALB/c. nu/mu recpiients, evidence was obtained for a defect in the thymus of young male mice and conceivably this defect may extend to the peripheral T cell population in such mice. Cyclophosphamide pretreatment or adrenalectomy increased circulating reagin titers in normal mice dosed intranasally with ABF + BPV, and pretreatment with lipopolysaccharide intranasally markedly reduced titers of circulating anti-ABF reagins. In the discussion, emphasis is given to the hypothesis that potent allergens are T cell-stimulating, relatively persistent antigens which, when located in submucosal lymphoid sites and under conditions of limited antibody production as a result of limited recruitment of 'helper' T cells systemically, lead to the induction and sustained production of IgE by resident Bxi cells and their progeny.

Adrenalectomy↗
PubMed1981

Effect of histamine agonists and antagonists on the production of murine reaginic antibodies.

At least wo histamine receptors have been pharmacologically defined. Using the appropriate agonists and antagonists, the possible involvement of these receptor types in the production of reaginic antibodies in the rodent was investigated. After injecting mice with dinitrophenyl-ovalbumin (DNP-OA), maximal serum reaginic titers occurred on day 11 as measured by heterologous passive cutaneous anaphylaxis. If the mice were dosed daily (i.p.) with the H1 agonist, 2-methylhistamine, or the H2 antagonist, metiamide, the titers of reaginic antibodies on day 11 were significantly higher than the controls. The titers were significantly lower than the controls if an H2 agonist (4-methylhistamine, dimaprit, or impromidine) or if the H1 antagonist, pyrilamine, was administered daily. None of these agents significantly affected total serum IgG titers as measured by ELISA. However, if the mice were injected with DNP-OA on day 0, then dosed daily with metiamide, pyrilamine, or 4 methylhistamine beginning on day 32, the titers of reaginic antibodies elicited by a second injection of DNP-OA given on day 36 were not significantly different from the titers of the non-drug treated mice. Thus, under these conditions, with these agents, the results suggest that histamine receptors may be involved in modulating the production of reaginic antibodies during a primary immunological response, H1 receptor agonists enhanced, while H2 receptor agonists suppressed the responses, and the reverse effect was observed with the appropriate antagonists. However, histamine receptors appear not to be measurably involved in the development of the secondary reaginic response.

Animals↗
PubMed1975

Correlation of anaphylactic bronchoconstriction with circulating reaginic antibody level and active cutaneous anaphylaxis in the rat.

The interrelationships of anaphylactic bronchoconstriction, active cutaneous anaphylaxis and circulating reaginic antibody level in rats sensitized with Nippostrongylus brasiliensis have been studied. The mean rise in bronchial reactivity during the 5-week sensitization period was correlated with the rise in circulating reaginic antibody level in groups of rats, although weak bronchial reactivity was observed before circulating reagin was demonstrable. In individual animals bronchial reactivity did not significantly correlate with circulating reaginic antibody level or cutaneous reactivity. Bronchial and cutaneous reactivity on challenge may be transferred to non-sensitized rats by passive sensitization with reaginic serum. It is concluded that the ability of a tissue to respond to antigen challenge is multifactorial and may not be reliably predicted from a knowledge of circulating reaginic antibody level or the response of another tissue in the same animal.

Anaphylaxis↗
PubMedDate not supplied

Immunogenicity of fungi for the production of reaginic antibody in the rat.

Immunogenicity of culture filtrates of various air-born fungi with respect to reaginic antibody formation was tested in the rat. Animals immunized with two successive injections of culture filtrates of fungi with the aid of Bordetella pertussis vaccine as an adjuvant produced fairly high titers of reaginic antibodies of the IgE class. Little cross-reactivity was detected between reagins induced by different strains of fungi. The reaginic immunogenicity was only found in the culture fieltrate produced by the surface culture, in which large amounts of conidia were formed, but not in the filtrate obtained from the shaking culture, in which only mycelial components were growing. Therefore, it was suggested that allergens responsible for the reaginic antibody formation derive from the conidium but not from the mycelium. The results indicate that air-born fungi are potentially immunogenic for production of reaginic antibodies, and further suggest their causative roles in human atopic diseases.

Adjuvants, Immunologic↗