The interaction between the cellular components of the intestinal mucosa and its lumenal environment has been studied in the piglet with the objective of establishing an early onset of secretory antibodies against pathogenic E. coli.
Morphological evaluation of the mucosal architecture during development showed that inflammatory changes occur in apparently healthy suckling piglets as early as 10 days after birth. These changes, which become progressively more severe as the animal ages, are greatly exacerbated by E. coli infection. The proximal small bowel is the area most affected, indicating that protective immune function should be preferentially directed towards this region.
A quantitative evaluation of macromolecular absorption at different levels of small intestine, using both horse-radish peroxidase and E. coli endotoxin indicated that uptake was
greatest in the anterior small bowel and that the rate of absorption decreased with age. Uptake of one macromolecule was not affected by the presence of the other suggesting lack of competition for binding sites on the absorptive epithelium.
Immunofluorescent studies on intestinal mucosa of pigs of varying age demonstrated IgM containing cells in duodenal lamina propria of 2 day old animals. IgM cells continued to out number IgA and IgG cells until the animals were weaned at 3 weeks old, thereafter IgA cells predominated.
In vitro evaluation of intestinal secretory antibody production in response to oral immunization showed specific antibodies in 14 day old pigs immunized from 4 days old. The greatest response was obtained from the anterior small bowel, again emphasising the importance of this region.
The protection conferred by early oral vaccination was determined, in vivo, in piglets experimentally infected with enteropathogenic E. coli and weaned at 14 days of age. The faecal E. coli count of the vaccinated group was reduced 100 fold compared to the placebo group and their weight gain after 1 week was 15% greater. The implications of these findings are discussed
