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At least 991 records · Page 55Linked to original sources
PubMed1983

Giardia lamblia infection of suckling mice.

Axenically cultured Giardia lamblia trophozoites (2 x 10(5)) were inoculated by gavage into suckling mice. All mice three, seven, and 14 days old became infected, with the peak trophozoite count in the small bowel of 5.3 +/- 1.1 x 10(6) occurring seven days after inoculation of three-day-old mice. In addition to infecting each of 65 challenged mice, G. lamblia was able to complete its life cycle by encysting and, as cysts, to infect previously unchallenged animals. Control mice given culture medium alone, mice challenged with trophozoites when older than 14 days of age, and mothers of infected mice did not become infected. There was no difference in body weight between infected mice and control mice, nor were histopathologic changes in the small bowel noted at the time of peak infection. Infection was cleared in all mice by 17-21 days. Thus, axenically cultured G. lamblia trophozoites are capable of infecting and completing their life cycle in suckling mice. The susceptibility of mice to infection is remarkably age specific, and the infection is apparently without adverse effects on the murine host.

Aging↗
PubMed1983

Giardia lamblia infections in Mongolian gerbils: an animal model.

Mongolian gerbils were susceptible to infection with Giardia lamblia cysts from patients. Inoculation of gerbils with 5 x 10(3) cysts each resulted in an infection characterized by the intermittent release of cysts for up to 39 days. The mean number of cysts released per gerbil in a 2-hr period was 8.8 x 10(2) (range, 0-5 x 10(3)). The highest number of trophozoites found in the intestine was on day 15 after infection, when the mean number of trophozoites per gerbil was 6.36 x 10(6). Administration of cysts from different patients to gerbils resulted in a similar pattern of cyst release during the first 30 days of infection. Mongolian gerbils were also susceptible to infection with cultured trophozoites (Portland 1 strain). The pattern of cyst release and the number of trophozoites in the intestines of orally and duodenally inoculated gerbils were similar. Gerbils were protected against reinfection with G. lamblia for up to eight months after primary infection.

Animals↗
PubMed1997

Mucosal abnormalities in microsporidiosis.

OBJECTIVE: To determine the prevalence of microsporidiosis in HIV-infected patients with and without diarrhoea and to characterize alterations in mucosal architecture and brush border enzyme activities in patients with microsporidiosis. PATIENTS: A total of 259 HIV-infected patients undergoing oesophago-gastroduodenoscopy because of diarrhoea (n = 123) or other symptoms (n = 136) were studied. METHODS: Patients were evaluated for the presence of microsporidia by electron microscopy of duodenal biopsies. Brush border enzyme activities were measured by histochemistry and mucosal architecture was determined by three-dimensional morphometry in biopsies from patients with microsporidiosis and compared with biopsies from a subgroup of HIV-infected patients with or without other enteropathogens. RESULTS: Enterocytozoon bieneusi was detected in 17 patients and Encephalitozoon intestinalis was detected in two patients. Microsporidiosis was significantly more frequent in patients with chronic diarrhoea (19.1%; P < 0.0001) or in patients with acute diarrhoea (7.2%; P = 0.04) than in patients without diarrhoea (1.5%). Microsporidiosis was associated with lactase deficiency (P = 0.03) and a reduced activity of alkaline phosphatase (P = 0.028) and alpha-glucosidase (P = 0.025) at the basal part of the villus compared with brush border enzymes in patients without enteropathogens. Patients with microsporidia had reduced villus height (P = 0.043) and a villus surface reduced by 40% (P = 0.004) compared with patients with enteropathogens other than microsporidia. CONCLUSIONS: Our study confirms the association between microsporidia and diarrhoea. The pathophysiologic mechanism by which microsporidia cause diarrhoea appears in part to be malabsorption, caused by a reduction of absorptive mucosal surface and impairment of enterocyte function.

AIDS-Related Opportunistic Infections↗
PubMed1991

Reconstruction of immune-mediated ion secretion in gut mucosa of the athymic rat.

A defect in an immune-mediated, physiological reaction in the small intestine of congenitally immunosuppressed rats has been identified and corrected by recoupling the immunological trigger in the mucosa with epithelial effector cells. Antigenic challenge of jejunum from euthymic rats sensitized by infection with Trichinella spiralis evoked an anaphylactic response in vitro that was characterized by an elevation in transmural short-circuit current (Isc) and caused by net Cl- secretion. In contrast, jejunum from previously infected athymic counterparts failed to respond electrophysiologically to antigenic stimulation. Passive immunization of athymic rats with anti-Trichinella serum restored jejunal responsiveness to antigen. Jejunal unresponsiveness to antigenic challenge in the athymic rat compared with the euthymic rat was not due to a difference in the duration of exposure to the sensitizing antigens, mast cell numbers, inflammation-related histological changes nor to reduced responsiveness of epithelium to Cl- secretagogues. Because the transduction of the antigenic signal into epithelial ion transport changes in euthymic rats requires IgE, mucosal mast cells, mast cell-derived mediators and enteric nerves, the results support the conclusion that an antibody deficiency is the only functional defect preventing the antigen-induced change in mucosal ion transport in the athymic host.

Animals↗
PubMed1994

Strongyloides venezuelensis infection in Syrian golden hamster, Mesocricetus auratus, with reference to the phenotype of intestinal mucosal mast cells.

Syrian golden hamster, Mesocricetus auratus, was found to be a moderately susceptible host for the intestinal helminth, Strongyloides venezuelensis. After infection by subcutaneous inoculation with 3000 infective larvae (L3), about 20% of them became adult worms in the small intestine, and, after a stable infection up to day 20, adult worms were slowly and gradually expelled towards day 45. Before infection, mast cells in the jejunum were about 30/10 villus crypt units and over 80% of them were formalin-resistant and berberine sulphate-fluorescence positive. After infection with S. venezuelensis, the number of intestinal mast cells gradually increased with time and about a half of them were formalin-sensitive and berberine sulphate fluorescence-negative. Intraepithelial migration of mast cells was never seen before and after infection. Heterogeneity of mucosal mast cells in terms of granular proteoglycans was further confirmed by the determination of critical electrolyte concentration. In spite of the heterogeneity of proteoglycans, enzyme-histochemical study revealed that practically all mucosal mast cells of Syrian golden hamsters were positive for chymase but negative for tryptase. Mast cells in the skin and tongue were also positive for chymase but negative for tryptase. Together with our previous study on mucosal mast cells of other rodents, phenotypic variances of mucosal mast cells seem to be closely related to the protective capacity against the genus Strongyloides.

Animals↗
PubMed1994

Expulsion of Hymenolepis nana from mice with congenital deficiencies of IgE production or of mast cell development.

The roles of IgE and mast cells on expulsion of adult Hymenolepis nana from the intestine were examined in mice. IgE-dependency was determined by comparing congenitally IgE-deficient SJA/9 and IgE-producing SJL/J mice infected with 50 H. nana eggs. Anti-H. nana IgE antibody was detected at three weeks post infection (p.i.) in SJL but not in SJA mice. The number of adult worms in the intestines of SJA and of SJL mice were similar at two weeks, but significantly more were found in SJA mice at three weeks p.i. Treatment of mice with anti-epsilon antibody also resulted in an increased worm burden at three weeks, suggesting participation of IgE in expulsion of H. nana. Intestinal mastocytosis was induced by infection regardless of the IgE status of the mice. Mast cell-dependency was tested in mast cell-deficient W/Wv and in normal littermate +/+ mice infected with 100 H. nana eggs. Anti-H. nana antibody was detected in both groups of mice at three weeks p.i. Worm expulsion seemed to be mast cell dependent because expulsion was less complete in W/Wv mice at three weeks p.i. Peripheral blood eosinophilia was comparable at three weeks p.i. in both IgE and mast cell sufficient and deficient mice. These results suggest that IgE and mast cells participate in the expulsion of H. nana adults from intestine in mice.

Animals↗
PubMed1994

Reconstitution by bone marrow grafting of the defective protective capacity at the migratory phase but not at the intestinal phase of Nippostrongylus brasiliensis infection in W/Wv mice.

After a primary infection by subcutaneous inoculation with the infective larvae (L3) of Nippostrongylus brasiliensis, the intestinal worm burden was higher and expulsion was slower in W/Wv mice than in +/+ mice. When the course of infection was segregated into the migratory and intestinal phases, protection during the migratory phase examined by the larval recovery from the lungs and that during the intestinal phase measured by worm burden after intraduodenal implantation with adult worms were both defective in W/Wv mice. The higher susceptibility of W/Wv mice during the migratory phase was normalized by bone marrow reconstitution. On the other hand, higher susceptibility of W/Wv mice during the intestinal phase, which was measured by worm burden 24 h after intraduodenal implantation of the larvae recovered from the lungs of rats, was not normalized by bone marrow grafting. Furthermore, slower expulsion seen in W/Wv mice after intraduodenal implantation with adult worms was not hastened by bone marrow reconstitution. These results indicate that the protective mechanisms against N. brasiliensis operating during the migratory phase and those during the intestinal phase were different in terms of bone marrow dependency and that non-myeloid cells utilizing c-kit ligand/receptor system to express their functions are involved in the mucosal defence against N. brasiliensis.

Animals↗
PubMed1995

Effect of testosterone on the mucosal defence against intestinal helminths in Indian soft-furred rats, Millardia meltada with reference to goblet and mast cell responses.

Effects of testosterone on the mucosal defence mechanisms against intestinal helminths were examined in Millardia meltada. When female M. meltada were treated with testosterone at the pharmacological dose, Nippostrongylus brasiliensis infection persisted for over seven weeks with prominent biphasic pattern of faecal egg production, whereas almost complete expulsion was observed by two weeks in untreated controls. In spite of a biphasic pattern of faecal egg production, the worm burden of testosterone-treated animals remained constant up to three weeks and then slowly decreased by seven weeks. To see whether or not this delayed expulsion in testosterone treated animals was due to altered cellular responses of the intestinal mucosa, goblet and mast cell responses were examined histologically. At two weeks post-infection, goblet cell responses at the infected site were significantly lower in testosterone-treated animals than in controls. In contrast mast cell hyperplasia was comparable between testosterone-treated and control animals. When Strongyloides venezuelensis, in which expulsion is dependent on mucosal mast cells, were infected concurrently with N. brasiliensis, testosterone-treated animals could expel S. venezuelensis worms by Day 18, but failed to expel N. brasiliensis. Histologically, mast cell hyperplasia was associated with expulsion of S. venezulensis, while goblet cell responses were suppressed. From these results, testosterone seems to suppress proliferation/function of goblet cells but does not affect mast cells of M. meltada.

Animals↗
PubMed1995

Reduced amount of intestinal mucus by treatment with anti-CD4 antibody interferes with the spontaneous cure of Nippostrongylus brasiliensis-infection in mice.

Mechanism of spontaneous cure was studied in mice infected with mouse-nonadaptive Nippostrongylus brasiliensis. Adult BALB/c mice were cured spontaneously of infection with this strain of N. brasiliensis by Day 7 post-infection. Expulsion of intestinal worms was delayed dose-dependently by a treatment with anti-CD4 antibody. However, the treatment had no significant effect on larval recovery from the lungs. Treatment of mice with anti-IL-5 antibody suppressed intestinal tissue eosinophilia induced by the infection, but did not affect intestinal worm recovery. Antigen specific IgE antibody was not detected in the sera obtained from Days 5 to 15. Therefore, IL-5 and specific IgE antibody are probably not important in the spontaneous cure. Treatment of mice with anti-CD4 antibody had no significant effect on number of intestinal goblet cells or on expression of terminal sugars of goblet cell mucins. However, histological and quantitative analyses revealed that significantly less intestinal mucus was released in anti-CD4 antibody treated mice than in control mice. These results suggest that CD4+ lymphocytes control the amount of intestinal mucus and consequently the reduced mucus interferes with the spontaneous cure. Quantity of mucus released in the intestinal lumen may have an essential role in the spontaneous cure of N. brasiliensis-infection of mice.

Animals↗
PubMed2006

The role of TGF-beta in mice infected with Heligmosomoides polygyrus.

Hyporesponsiveness induced by Heligmosomoides polygyrus was quantified and the relationship between TGF-beta and inflammation was identified in BALB/c mice. The immune response and pathological changes modified by neutralization of TGF-beta were characterized in vivo. Nine and twelve days following infection, BALB/c mice were injected intraperitoneally with anti-TGF-beta (1,2,3) antibodies, isotype control antibodies or isosmotic solution. We assessed both Th1 and Th2 related cytokines production ex vivo and in vitro, IgA, the number of CD4+ cells, and eosinophils in the lamina propria and the villus : crypt ratio in the small intestine 6 weeks after infection. The pattern of cytokine production differed in the intestine, peritoneal fluid and serum. In mice infected with H. polygyrus the concentrations of IL-5, IL-12, TNF-alpha and IL-10 were raised in the intestine, but in serum the level of cytokines was diminished below the value observed in uninfected mice. The neutralization of TGF-beta converted the pattern of immune response induced by H. polygyrus. The elevation of cytokines in serum coincided with the reduction of cytokine concentration in the intestine or peritoneum. Neutralization of TGF-beta restored infiltration of eosinophils into the lamina propria of the intestine despite the low level of IL-5. We conclude that H. polygyrus infection suppresses the immune response through pathways involving TGF-beta production or activity and that the Th2 related immune response was not affected by neutralization.

Animals↗