Pathogenesis of swine dysentery: The role of luminal antigens in the activation of mucosal T lymphocytes

Changes in the diet of swine have been speculated to be a factor which can precipitate swine dysentery. The effect of diet alteration was examined using a mouse model for S. hyodysenteriae infection. Altering the diet of mice resulted in the appearance and waning of cecal lesions dependent upon which diet was being fed to the mice. This effect could not be attributed to altering levels of S. hyodysenteriae.;Previous studies using gnotobiotic animals infected with Serpulina hyodysenteriae have demonstrated that without the presence of the intestinal microflora, S. hyodysenteriae is unable to cause disease in susceptible animals. The intestinal microflora's contribution was previously hypothesized to be providing factors which facilitated the colonization of S. hyodysenteriae in the colon. The contribution of the intestinal microflora to disease pathogenesis was examined by evaluating the numbers of S. hyodysenteriae and the numbers of intestinal bacteria present in the colon of mice in a model which mimics the gnotobiotic phenomenon (i.e., colonization without lesion induction). Oral administration of antibiotics via the drinking water renders mice free from intestinal inflammation caused by S. hyodysenteriae. A decrease in the numbers of S. hyodysenteriae was not detected in the colon of these animals thus, the effect was likely due to a reduction in the levels of the intestinal microflora. However, the numbers of intestinal microflora were found unchanged following treatment. The effect was hypothesized to be the result of a reduction in the numbers of Gram negative anaerobes present in the colon.;S. hyodysenteriae infection results in severe inflammation of the colon of affected animals. The contribution of immune cells to the inflammation, specifically T lymphocytes, present in the mucosal tissue was examined. Evidence of phenotypic T lymphocyte activation was not noted during acute S. hyodysenteriae infection although these cells were functionally active (i.e., enhanced cytokine secretion). T lymphocytes isolated during chronic stages of the disease were phenotypically and functionally active. Functional activity could be enhanced by stimulation with antigens representative of the intestinal microflora. Thus, T lymphocytes may contribute to the chronicity of the inflammation via cytokine secretion following stimulation by antigens derived from the intestinal microflora.