Lamina Propria Of Rats Research Articles

New method for isolation of rat lamina propria macrophages in colonic tissue

Studies on intestinal cells in the lamina propria are important for understanding the cellular and immune responses in the gut. There is a lack of specific isolating procedures of macrophage cells in rats. Two different procedures of macrophage isolation of the lamina propria in rats are compared: a standard mice protocol for lymphocyte isolation (A) adapted to rat samples and a new protocol developed specifically for rats (B). Significant differences are observed when analyzing the effect of the isolation method on the cell number, viability and phenotype. This has important implications when further functional studies are required.

Immunohistochemical quantitative study of the peritubular lamina propria after induction of testicular atrophy induced by epinephrine.

Changes in the testicular peritubular lamina propria in rats treated for 1-11 weeks with intra-scrotal injections of epinephrine were studied by quantitative immunohistochemical methods. In control testes, BrdU-labelled nuclei (proliferating cells) were observed only in spermatogonia and some primary spermatocytes, whereas testes from epinephrine-treated rats showed BrdU labelling in some of the spermatogonia and in peritubular cells. Immunostaining for transforming growth factor beta 1 (TGF-beta 1) was present in germ cells, Sertoli cells and Leydig cells; vimentin immunostaining was found mainly in Sertoli cells; desmin immunostaining was found in the peritubular cells, and immunostaining for type IV collagen, laminin and fibronectin was found in the extracellular matrix of the lamina propria. The volume densities of seminiferous tubules (including seminiferous epithelium, lamina propria and tubular lumen) that immunostained for TGF-beta 1, vimentin, laminin, desmin or fibronectin were calculated. All of these parameters increased significantly in testes from epinephrine-treated animals during the course of the experiment, except for desmin immunostaining which showed no significant change in volume density. Since total seminiferous tubule volume decreased markedly in the testes of treated rats during the experiment, the transformation of relative values for immunostaining into absolute volumes per testis revealed a significant increase in TGF-beta 1 immunostaining, no significant change in vimentin immunostaining, and a significant decrease in desmin immunostaining during the time of the study. The absolute volume occupied by laminin and fibronectin immunostaining decreased from the 3rd to the 8th weeks of treatment, and increased from the 8th to the 11th weeks. These changes, associated with germ cell depletion and tubular fibrosis, suggest that tubular ischaemic atrophy caused by epinephrine alters the peritubular myoid cells, which change immunophenotype and increase their secretion of the extracellular matrix components producing tubular fibrosis. The mechanism of this alteration may involve direct effects on the peritubular cells or the changes may be secondary to germ cell and/or Sertoli cell lesions.

Ultrastructure of the epithelial cells of the small intestinal villi, the surface epithelium of the large intestinal mucosa and some elements of the intestinal mucosal lamina propria in rats with acute uraemia

Electron microscopic studies on the dynamics of changes in the epithelial cells and some elements of the intestinal mucosal lamina propria were performed on rats after bilateral high ureter ligation. Simultaneously, they were referred to blood serum biochemical and electrolyte disturbances. The ultrastructural changes indicate that as early as in the initial period of acute uraemia water-electrolyte disturbances become evident, which are still increasing. In the later period cell organelles alter and bacterial infection sets in. Ultrastructural abnormalities of the intestinal mucous membrane are increasing proportionally to biochemical and electrolyte disturbances of the blood serum.

Immune response of the intestinal mucosa to cholera toxoid.

The intestinal immune response to cholera toxoid was studied in dogs and rats. Oral or intraperitoneal priming followed by duodenal boosting with toxoid reulted in antitoxin-containing plasma cells (ACC) in jejunal lamina propria of rats. Priming and boosting by the intraperitoneal route alone induced almost no jejunal response. Lamina propria ACC were derived largely from migrating immunoblasts, which appeared earlier among thoracic duct lymphocytes. Protection of dogs after repeated subcutaneous immunization with toxoid was mediated largely, or entirely, by serum-derived antibody. The sequence of subcutaneous priming and repeated oral boosting induced longer lasting protection mediated almost entirely by the local intestinal immune mechanism. The results suggest that cholera immunization should be specifically designed to stimulate the intestinal immune mechanism and that the subcutaneous oral immunizing sequence may be an efficient way to do this.