Disaccharidase activity in the small intestine of gerbils (Meriones unguiculatus) during primary and challenge infections with Giardia lamblia.

Abstract

SUMMARY The sequence of changes in the activity of six disaccharidases in the small intestine of gerbils during primary and secondary G lamblia infections was examined. The primary G lamblia infection induced a transient reduction in disaccharidase activity which was related to the highest trophozoite burden in the small intestine. During the primary exposure, a 30% to 85% decrease in the activity of enzymes was observed on days 10 and 20 after infection. Secondary exposure of gerbils to G lamblia caused a sharp decrease in disaccharidase activity as early as 24 h after challenge. The reduction in the enzyme activity was not influenced by the size of the challenge inoculum and occurred even when there were no live trophozoites in the small intestine. Disaccharidase deficiency could also be induced by challenge with the soluble extract of the trophozoites. Multiple challenge administrations of G lamblia trophozoites to gerbils induced a persistent disaccharidase deficiency. The results indicate that disaccharidase deficiency associated with the primary G lamblia infection probably represents a direct effect of the parasite on the brush border of the small intestine. On the other hand, the observed disaccharidase deficiency in the secondary G lamblia infection appears to be induced by the local immune responses of the host.Various abnormalities of small bowel pathology have been identified consistently in human giardiasis and these include disaccharidase deficiencies,' 2 increased intraepithelial lymphocyte counts'4 and, in patients with malabsorption crypt hyperplasia with short villi and increased lamina propria cellularity.) Low serum calcium and folate concentrations were consistent features in elderly people having giardiasis and aroused suspicion of underlying malabsorption." A decrease in the disaccharidase activity has been observed in vitro. Mouse mucosal cells incubated with G lamblia trophozoites showed a reduction in the activities of lactase, sucrase, and maltase.7We have recently described an animal model for giardiasis using gerbils and G lamblia isolated from humans.' In this study, we examined the progression

Lactobacillus johnsoniiLa1 AntagonizesGiardia intestinalisIn Vivo

“…The present in vivo study consolidates recent reports describing the capacity of some lactobacilli of human and canine origin to antagonize Giardia infection which interferes with the growth and cell cycle of G. intestinalis in vitro (36). Mongolian gerbils (Meriones unguiculatus) are a good animal model for studying Giardia infection with strains of human origin (3,4,11). Their susceptibility to giardiasis has been attributed to a deficient antibody response to specific Giardia antigens (34).…”

“…Intestinal disaccharidase activity was determined as previously reported (16). Protein concentrations were determined using the Bradford assay, and the results are expressed as arbitrary units per gram of protein (3).…”

Immunopathology of giardiasis: the role of lymphocytes in intestinal epithelial injury and malfunction

“…First, in immuno-competent but not in T-cell deficient animals, acute giardiasis causes a diffuse loss of epithelial brush border surface area and decreases sucrase and maltase activities (Scott et al 2000). During the acute phase of the infection, epithelial abnormalities were not seen in the jejunum of Gupta et al 1973, Chawla 1975, Ducombe et al 1978, Gillon et al 1982, Faubert 1988, Belosevic et al 1989, 1992, Favennec et al 1991, Katelaris et al 1991, Cevallos et al 1995, Mohammed et al 1995, O'Handley et al 2001 athymic mice, despite comparable parasitic loads to those seen in immuno-competent animals, implying that the lack of microvillous injury could not be attributed to a reduction in trophozoite numbers. Second, experiments using in vivo T lymphocyte transfer into naïve animals demonstrate that brush border injury and malfunction in giardiasis are mediated by CD8 + T lymphocytes, while CD4 + T lymphocytes are responsible for parasite clearance (Scott et al 2004).…”

“…Recent studies have found that CD8+ lymphocyte adhesion to epithelial cells via α E β 7 contributes to the destruction of pancreatic islet cells (Butcher et al 1996, Feng et al 2002. Previous reports have also shown that secondary challenge with fractions of G. duodenalis trophozoites may cause disaccharidase deficiencies in the absence of live parasites (Belosevic et al 1989). The signaling events implicating CD8 + T cells, integrins like α E β 7, and possibly TGFβ , in the brush border injury during giardiasis and other disorders of the intestine warrant further investigations.…”

SGLT-1-mediated glucose uptake protects human intestinal epithelial cells against Giardia duodenalis-induced apoptosis

“…Studies in human patients, in experimental animal models, or in cell culture systems, have established that the infection causes small intestinal structural and functional abnormalities. These may include apoptosis induced epithelial barrier defects, microvillous shortening, disaccharidase deficiencies, hypersecretion of chloride, as well as malabsorption of electrolytes and water associated with infiltration of intraepithelial lymphocytes ( [Belosevic et al, 1989], [Buret et al, 1992], [Scott et al, 2000], , [Scott et al, 2004], [Troeger et al, 2007] and [Panaro et al, 2007]). …”