PubMed · 4979910
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T Suzuta. 1969. [Experimental method for allergy. 1].. https://pubmed.ncbi.nlm.nih.gov/4979910/
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The pathophysiological responses to immune stress (IS) include activation of several processes which are dependent on cytosolic Ca2+ elevation. Magnesium frequently acts as a natural Ca2+ antagonist. In this study we have observed that Mg2+ can protect guinea-pigs against IS. Antigen-sensitized guinea-pigs, which had been fed a magnesium-deficient diet, were given a single dose (15 mg) of MgCl2 intraperitoneally 1 h before antigen challenge. The development of anaphylactic shock (AS) was observed during the next 2 h, and the hearts were subsequently examined histologically for signs of cardiac myolysis (CM). Magnesium (i) reduced the incidence of CM from 40% to 10% (p < 0.05); (ii) reduced the incidence of AS from 61% to 35% (p < 0.05); (iii) attenuated the severity of the AS; and (iv) lowered mortality from 39% in the control to 19% in the Mg(2+)-treated group (p = 0.1). Serum and tissue total [Mg2+] were not affected by the administration of MgCl2. Also, the serum and heart Mg2+ levels were the same whether or not the guinea-pigs developed AS or CM. In cell culture we demonstrated that by elevating the [Mg2+] in the medium bathing sensitized rat basophilic leukemia (RBL) cells, the increase in cytosolic [Ca2+] subsequent to antigen challenge was reduced from 174 +/- 23.28% (1 mM) to 82.74 +/- 13.22% (3 mM). We conclude that a single treatment with Mg2+ can considerably diminish damage induced by immune stress, probably by its altering the Ca2+: Mg2+ ratio. Since the physiological reaction to different types of stress is similar, Mg2+ could prove beneficial in preventing stress-induced shock in general. Studies examining the mechanisms by which Mg2+ exerts its effects thus provide a scientific basis for the current clinical use of Mg2+ in acute myocardial infarction (AMI) and asthma.
The frequency of HLA class I and II phenotypes was determined among 23 patients with positive gelatin IgE, eight of whom developed anaphylaxis, 18 patients who did not have gelatin IgE but who experienced non-immediate reactions after exposure to gelatin. HLA-DR9, which is unique to Orientals, was present in 56.5% of the gelatin IgE positive patients, as compared to control population frequency of 24% (P < 0.002). In the non-immediate reaction group, who did not generate IgE, phenotype distribution resembled controls. HLA-DR9 positive individuals have a relative risk of 4.1 for developing gelatin allergy with positive IgE.
This study was performed to mimic human consumption of fish flesh infected with larvae of the fish cestode Gymnorhynchis gigas and examine possible side effects thereof. Both a rat and a mouse G. gigas oral inoculation model were used. The rat model was evaluated according to propensity to induce stress responses in three tissues and anaphylactic antibody production. The mouse model measured anti-G. gigas IgG, M and A (H + L) levels in intestinal fluids, fecal suspensions and serum and specific serum IgE levels by enzyme-linked immunosorbent assay. Additionally, biological activity of anaphylactic antibodies in test mice and rats were evaluated utilizing challenge reinoculation(s) and intradermal skin testing, respectively. With the rat inoculation model, we noted both occurrence of a shock response, viz. increased expression of heat shock proteins in intestine and spleen, and of immediate-type skin reactions. No positive wheals were seen on skin sites treated with PBS or soluble Trichinella spiralis extract. With the mouse model, our results showed that all body fluids tested had significantly more anti-G. gigas IgG, M and A (H + L) than their counterparts from either PBS-treated or T. spiralis-infected controls. In addition, the mouse G. gigas model had significantly higher specific serum IgE. When challenged by oral route all test mice (n = 5) manifested immediate-type signs of distress. Repeated exposure to the "allergen", produced clinical signs appearing more rapidly and persisting longer. These findings suggest that feeding on fish infected with G. gigas plerocercoids triggers the production of anaphylactic-type antibodies in both rats and mice and, by implication, possibly also in humans.