Antigen-Antibody Reaction in the Gastric Mucosa

Studies from the Standpoint of Complement and Plasmin

Abstract

Complement components are known to have important role in tissue damage caused with antigen-antibody reaction. Also, fibrinolytic activity is agreed to have its activity in the inflammed tissue. Studying the mechanism of antigen-antibody reaction in the gastric mucosa, following experiments are performed regarding with the complement and plasmin on "Passive mucosal anaphylaxis" and on experimental ulcer with soluble antigen-antibody complex.
1) Passive cutaneous anaphylaxis (PCA) was observed in the guinea pig and dog, with BSA-antiBSA system according to Ovary.
2) Applying the technique of PCA on the gastric mucosa of guinea pig and dog, interesting results were obtained; namely "Passive mucosal anaphylaxis" (PMA). In the course of PMA, marked edema, cell infiltration and bleeding in the gastric mucosa were observed within 2 to 12 hours after the challenge of antigen. But, neither ulcer nor erosio could be produced, even after the injection of gastrin to the dog with PMA.
3) Antigen was given orally to the dog injected the antibody in the gastric mucosa. PMA was observed only at the angle of stomach, while it was never observed when antigen was given in the small intestine.
4) When soluble antigen-antibody complex (Ag-Ab) was injected in the gastric mucosa of guinea pig and dog, it was observed to produce erosio and ulcer at the injected area within 2 hours. Histologically, chief cells were almost destroyed, while parietal cells were still partially remained at the damaged tissue.
5) Cell preparation of gastric mucosa were obtained with the treatment of trypsin, and coated with antiBSA antibody. These coated cells were reacted with BSA, complement and human red cells, and positive immune adherence phenomenon were observed. This fact might suggest the possibility of IA for detecting cell-bound antibody, or circulating antibody against gastric mucosa in atrophic gastritis and pernicious anemia.
As complement and plasmin system are known to be taking a part each other in the antigen-antibody reaction, the inter-relationship of both system is studied.
6) EACA and AMCHA (antiplasmin agents) inhibited PCA reaction in the guinea pig, to which complement components might take part in.
7) EACA and AMCHA inhibited complement activity measured with C'H₅₀ and IA in vitro, but did not inhibit in vivo with such a therapeutic dose.
8) Functionally pure human C₁ eluated from EAC₁₄, as well as euglobulin, showed fibrinolytic activity when activated by SK. This activity was decreased by mixing with EACA, AMCHA and Cu-chlorophyllin, treating with 56c°C for 30 minites, and also absorving with antigen-antibody complexes.
With these experiments, C₁ and plasminogen activator are supposed to have some interrelationship each other. Cell-bound C₁ and plasminogen tissue activator in the tissue with PMA are studied.
9) Cell-bound C₁ was titrated following the course of PMA, using the method of transferring to EAC₄. Tissue activator of plasminogen was measured according to Astrup's method. C'₁ and tissue activator showed parallel change in the time course of PMA.
10) Localization of C'₁ in the PMA tissue was studied by fluorescent antibody technique with anti-guinea pig C'₁ serum.
11) Cell-bound C'₁ and tissue activator in the experimental ulcer induced with antigen-antibody complex was titrated, and parallel changes were observed as in PMA. While no relationship could be observed in human gastric ulcer, except in one case of fresh ulcer which showed high C'₁ and tissue activator levels.