Role of Immunoglobulins G1 and G2 in Anaphylactic Shock in the Guinea Pig

Abstract

Heating serum from actively sensitised guinea pigs did not remove its ability to sensitise recipient animals in vivo and parenchymal lung strips in vitro to anaphylaxis. Thermoresistant antibodies should thus account for the transferable sensitising effect, which persists for at least 9 days. IgG1 and IgG2, contained in the serum, were separated by affinity chromatography to determine the importance and the participation of these subclasses in passive anaphylactic shock. IgG1, present in smaller amounts than IgG2, was more effective in sensitising isolated lung strips. The intravenous administration of ovalbumin to guinea pigs, which had been injected with 0.8 mg/kg of IgG1 or 2 mg/kg of IgG2 9 days beforehand, induced an intense bronchoconstriction with leucopenia and moderate thrombopenia, suggesting an as yet undescribed role for IgG2 in passive tissue sensitisation. The use of mepyramine, an antagonist of the histamine H₁ receptor, WEB 2086, an antagonist of platelet-activating factor, and nordihydroguaiaretic acid, a dual inhibitor of cyclooxygenase and lipooxygenase, alone or associated, demonstrated that the anaphylactic contraction of lung strips from guinea pigs sensitised by IgG1 is mediated by histamine and arachidonate derivatives, whereas that of lung strips from guinea pigs sensitised with IgG2 is mostly mediated by histamine. In addition, the association of the three potential antagonists slightly reduced the anaphylactic contraction of lung strips provided by guinea pigs sensitised by serum. Our results, using a sensitisation procedure considered until now to involve exclusively IgE antibodies, indicate that IgG1 and IgG2 are in fact the essential antibodies for passive anaphylactic shock in the guinea pig.

Interference of BN 52021, an antagonist of PAF, with different forms of active anaphylaxis in the guinea‐pig: importance of the booster injection

“…Nevertheless, lung strips may not be an adequate model for studying anti-allergic sub-stances. Indeed, using antagonists of the different mediators involved, we failed to suppress antigen-induced activation of lungs strips provided by passively (Desquand et al, 1991), or by actively sensitized guinea-pigs (Detsouli et al, 1985;Pretolani et al, 1987). As discussed below, inflammatory cell invasion of the lungs following the booster may account for the differences in sensitivity to PAF antagonists.…”

“…The sensitization procedure used by us involves the formation of a mixture of IgE and IgG (Andersson, 1980) and we recently demonstrated that the latter are more important for anaphylactic bronchoconstriction than the former (Desquand et al, 1991). To determine the possible relationship between the intensity of the immune response or the sub-class of immunoglobulins formed and the lack of effects of BN 52021, anaphylactic bronchoconstriction and the amounts of circulating IgG were studied over a period of time.…”

Mite-Induced Allergic Airway Inflammation in Guinea Pigs

“…These sensitized guinea pigs showed elevat ed serum D.farinae specific IgG antibody titer and severe anaphylactic bronchoconstriction after IV injection ofCME solution. We measured the D./a/7«ae-specific IgG antibody rather than the IgE antibody, as IgG antibody has recently been found to be the major anaphylactic immunoglobulin in guinea pigs [24][25][26][27], and the measurement of IgG antibody is easier in guinea pigs. The absence o f sensitization to mites by the inhalation method was different from that of the other commonly used allergen, ovalbumin, which can easily cause sensitization in animals by aerosol methods [7,23].…”

Specific IgE and IgG to gelatin in children with systemic cutaneous reactions to Japanese encephalitis vaccines

“…Some investigators have reported that IgG antibodies can act as a sensitizing antibody (19–21). In guinea pig, IgG1 and IgG2 are the essential antibodies for passive anaphylactic shock (22). Basophils and mast cells, besides FcεRI, have FcεRII or FcεRIII that binds IgG (23, 24), and basophils or mast cells can be activated through FcεRIII to release histamine (25).…”