The capacity of the stomach to participate in
anaphylaxis induced by the
hapten N,N'-di-2,4,dinitrophenyllysine (
di-DNP-lysine) was examined in BDF1 female mice immunized with dinitrophenylated Ascaris suum extract. Immunized animals underwent
laparotomy and nontraumatic pyloric occlusion using a microvascular clamp. Following
wound closure, animals were gavage-fed
ovalbumin together with
di-DNP-lysine. Other mice were subjected to systemic
anaphylaxis by
intravenous injection of
di-DNP-lysine administered 1 min after gavage feeding of
ovalbumin. The intravenous and intragastric administration of
di-DNP-lysine led to a sixfold or greater increase in serum immunoreactive
ovalbumin. Examination of 1-micron sections of gastric tissue from DNP-Asc-immunized and unimmunized mice showed an intact mucosal and submucosal architecture. A 75% increase in the number of mast cells below the muscularis mucosa was seen in immunized compared with unimmunized BDF1 mice. Gastric tissue sections from immunized mice challenged orally or intravenously with
di-DNP-lysine showed compaction of erythrocytes in blood vessels, degranulation of mast cells, degenerative changes in the gastric epithelium, expulsion of mucus from gastric glands, and
edema in the lamina propria. The present model may be useful for further defining the consequences of
anaphylaxis on the development of immune responses to dietary
antigens.