scholarly journals THE SPECIFICITY OF ALLERGIC REACTIONS

1961 ◽  
Vol 114 (2) ◽  
pp. 185-194 ◽  
Author(s):  
S. B. Salvin ◽  
R. F. Smith

Intradermal injection of a simple hapten (e.g., 1-fluoro-2,4-dinitrobenzene) in water-in-oil emulsion results in contact hypersensitivity to surface application of the homologous hapten and, after appearance of circulating antibody, in Arthus type hypersensitivity to a conjugate of homologous hapten with guinea pig serum. Intradermal administration of this conjugate induces delayed and subsequently Arthus hypersensitivity to the conjugate, but no evidence of a contact reaction to the hapten alone. When a conjugate of hapten plus solubilized guinea pig skin is used as the sensitizing antigen, both contact hypersensitivity to the hapten and delayed and/or Arthus reactions to the conjugate develop. These observations are consistent with the hypothesis that the specificity of contact sensitivity is directed toward some particular protein of the skin which has been modified by combination with hapten.

1955 ◽  
Vol 101 (6) ◽  
pp. 591-604 ◽  
Author(s):  
Jules Freund ◽  
George E. Thompson ◽  
Murray M. Lipton

Guinea pig testicles were extracted with acetic acid; the extract was purified by removing material in consecutive precipitations with 30 per cent saturated ammonium-sulfate, trichloracetic acid, and chloroform. The solution so purified, when administered with complete adjuvants, was highly active in inducing impairment of spermatogenesis in guinea pigs. The activity resisted autoclaving at 15 pounds' pressure for 20 minutes, proteolytic enzymes, and formamide. Anaphylactic shock and cutaneous reaction to the purified homologous extract occurred in guinea pigs sensitized by the extract combined with adjuvants. For the production of aspermatogenesis it was essential to incorporate killed mycobacteria into the water-in-oil emulsion containing the antigen; but anaphylactic sensitization did not require the presence of mycobacteria.


1988 ◽  
Vol 168 (5) ◽  
pp. 1685-1698 ◽  
Author(s):  
C J Strang ◽  
S Cholin ◽  
J Spragg ◽  
A E Davis ◽  
E E Schneeberger ◽  
...  

Synthetic peptides that correspond to the COOH-terminal portion of C2b enhance vascular permeability in human and guinea pig skin. In human studies, 1 nmol of the most active peptide of 25-amino acid residues produced substantial local edema. A pentapeptide and a heptapeptide corresponding to the COOH-terminal sequence of C2b each induced contraction of estrous rat uterus in the micromole range; a peptide of 25 amino acids from this region induced a like contraction of rat uterus at a concentration 20-fold lower than the smaller peptides. The vascular permeability of guinea pig skin was enhanced by doses of these synthetic peptides in a similar fashion as that observed for the concentration of rat uterus. The induction of localized edema by intradermal injection in both the guinea pig and the human proceeds in the presence of antihistaminic drugs, suggesting that there is a histamine-independent component to the observed increase in vascular permeability. Cleavage of C2 with the enzymic subcomponent of C1, C1s, yields only C2a and C2b, and no small peptides, whereas cleavage of C2 with C1s and plasmin yields a set of small peptides. These plasmin-cleaved peptides are derived from the COOH terminus of C2b, and they induce the contraction of estrous rat uterus.


1953 ◽  
Vol 97 (5) ◽  
pp. 711-726 ◽  
Author(s):  
Jules Freund ◽  
Murray M. Lipton ◽  
George E. Thompson

The injection into the dorsal skin of a suspension of guinea pig testis or spermia incorporated in a water-in-oil emulsion containing killed mycobacteria induces aspermatogenesis in guinea pigs. The injury begins with the inhibition of the maturation of spermia and proceeds through the degeneration and exfoliation of spermatids, spermatocytes, and finally spermatogonia. These germinal cells pass from the seminiferous tubules into the epididymis. The process is not associated with inflammation. No significant changes occur in the intertubular spaces and the Leydig cells do not seem to be affected. The seminal vesicles and the prostate remain normal. The aspermatogenesis may begin in 10 days and it lasts for more than 5 months. The process may lead to atrophy of the seminiferous tubules and fibrosis. Guinea pigs which receive a suspension of their own testis or spermia and adjuvants develop a similar injury. The "mitochondrial" fraction of the testis of guinea pig is effective while repeated injections of alcoholic extract of testis emulsified with paraffin oil containing mycobacteria do not cause aspermatogenesis. The presence of acid-fast bacilli in the water-in-oil emulsion containing testis or spermia seems to be essential for the production of testicular lesions; the injection of antigen and mycobacteria into different sites is ineffective. When guinea pig testis is replaced by guinea pig liver or kidney or rabbit testis no testicular damage occurs. The injection of rabbit spinal cord combined with adjuvants results in allergic encephalomyelitis in a large proportion of guinea pigs, accompanied by a great loss of weight. The testes of a few of these animals show a varying degree of aspermatogenesis. When guinea pig brain is combined with adjuvants and administered subcutaneously the incidence of testicular injury is high, although the damage is, in general, mild. From the standpoint of mechanism, the inhibition of spermatogenesis which occurs in these animals may be unrelated to the injury which follows the injection of germinal cells. Aspermatogenesis follows the injection of killed mycobacteria in paraffin oil into the testis as well as into certain sites related to the gonad: the abdominal cavity, the subcutaneous tissue over the abdomen, and the skin of the inguinal region. Antibodies fixing complement in the presence of spermia are demonstrable in the sera of guinea pigs injected with testis or spermia and adjuvants. When the mycobacteria are omitted the titers are low and no testicular injury occurs. Although there seems to be a correlation between testicular damage and complement-fixing titer, this may not be a causal relationship. Antibodies which neutralize guinea pig hyaluronidase and those which immobilize spermia have also been demonstrated in the sera of these guinea pigs.


1964 ◽  
Vol 120 (5) ◽  
pp. 925-942 ◽  
Author(s):  
S. Ben-Efraim ◽  
B. Cinader

Intradermal injection of mice with ribonuclease antibody, followed by intravenous injection with ribonuclease, resulted in permeability increase, demonstrable by "blueing." The size of the blued area depends on the quantity of antibody injected and on the interval between the two injections. If antigen was injected first and antibody was injected subsequently, a similar increase in permeability was observed in animals having a complete complement system (MuB1-positive) and in animals which have a deficient complement system (MuB1-negative). Marked differences in response were observed between these two types of mice if antigen was injected some hours after the antibody. In MuB1-negative mice, a blueing reaction was not observed at intervals between injections (2½ hours if 3 µg N antibody and 15 hours if 25 µg N antibody were injected intradermally) at which MuB1-positive animals showed a marked permeability increase. At these intervals, blueing did occur in MuB1-negative animals if they were injected with the serum of MuB1-positive mice or with fresh guinea pig serum. Blueing was not induced if the serum of MuB1-negative mice or heated guinea pig serum was injected. The occurrence of two distinct phases of the cutaneous reaction, of which only one involves the complete hemolytic complement system, was deduced from these observations.


1936 ◽  
Vol 64 (4) ◽  
pp. 641-655 ◽  
Author(s):  
Marion C. Morris

1. Sensitized guinea pigs injected with normal rabbit or guinea pig serum previous to intravenous inoculation of antigen may be protected against a few lethal doses of antigen. The protection is greater with foreign than with homologous serum and appears to be related roughly to the amount of serum introduced. 2. Sensitized guinea pigs injected with antibody-containing serum preliminary to intravenous injection of antigen, show no greater refractoriness to anaphylaxis than do those injected with normal serum. 3. Moreover, in many instances, the injection of an excess of antibody into the circulation of sensitized guinea pigs, leads to an increased susceptibility of these animals to anaphylaxis. 4. These results indicate that an excess of circulating antibody is not responsible for a state of antianaphylaxis, but on the contrary, may contribute toward the anaphylactic reaction itself.


1957 ◽  
Vol 105 (1) ◽  
pp. 11-24 ◽  
Author(s):  
Jonathan W. Uhr ◽  
S. B. Salvin ◽  
A. M. Pappenheimer

A general method for induction of the delayed hypersensitive state directed against single protein antigens is described. The method consists of intradermal injection of minute amounts of washed immune precipitates containing the antigen in question. Provided the specific precipitates are formed in the region of antibody excess, maximal sensitivity develops at least 2 to 3 weeks before detectable circulating antibody is formed in guinea pigs against the sensitizing antigen. Neither adjuvant nor killed acid-fast bacteria are required for induction of the delayed hypersensitive state although the degree of sensitization is considerably increased when the sensitizing material is incorporated in Freund's complete adjuvant. Characteristics of the "delayed" as opposed to the "immediate" hypersensitive states in the guinea pig are described and implications of the findings are discussed.


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