Ischemic stroke damages the intestinal mucosa and induces alteration of the intestinal lymphocytes and CCL19 mRNA in rats.

The immunoreaction has a pivotal effect on ischemic stroke. It has been demonstrated that intestinal lymphocytes infiltrate into the brain and aggravate tissue injury after stroke. However, less attention has been paid to the influence on the intestinal immunology as well as morphology. Here, we utilized a rat permanent middle cerebral artery occlusion (MCAO) model to investigate the influences on intestinal mucosa, lymphocytes of the gut-associated lymphoid tissue (GALT), and the intestinal expression of CCL25 mRNA and CCL19 mRNA of stroke. Rats were randomly divided into stroke, sham, and control groups. Stroke and sham groups were further divided into interval groups of 6h, 12h, and 24h after surgery. Intestinal pathophysiological changes were observed by hematoxylin-eosin (H&E) staining. The lymphocyte numbers were detected by flow cytometry. The expression of CCL25 mRNA and CCL19 mRNA was tested with the PCR technique. We found significant necrosis and shedding of the epithelium after stroke. Moreover, the lesion aggravated with time. In addition, there was a significant increase of T lymphocytes in Peyer's patches (PPs), especially at 12h and 24h after stroke, while no differences in the number of B lymphocytes and the intraepithelial lymphocytes (IELs) were found. The data displayed no alteration of CCL25 mRNA expression. In contrast, an upregulation of CCL19 mRNA expression was detected at 6h after stroke. This study showed that ischemic stroke significantly damaged the intestinal epithelium and activated intestinal immunity.