Search PubMed⌕ Search

Biomedical subjects

M Shibayama-Salas

Publications and source records attributed to M Shibayama-Salas.

8 recordsLinked to original sources

Role of neutrophils in innate resistance to Entamoeba histolytica liver infection in mice.

In order to define the role of neutrophils in the innate resistance to Entamoeba histolytica liver infection in mice, we examined the pattern of liver lesion induced by direct injection of E. histolytica trophzoites in normal mice and in neutrophil-depleted mice. A variety of histological lesions were found, the extent of liver damage was considerably higher in the neutrophil-depleted mice. Livers from neutrophil-depleted mice displayed areas of liquefactive (lytic) necrosis containing a large number of amoebae and absence of neutrophils or mononuclear cells. By contrast, in the liver of normal mice, neutrophils were seen associated to E. histolytica at early stages of infection. In both mouse groups, areas of TUNEL-positive dead hepatocytes were observed and a characteristic internucleosomal banding pattern of genomic DNA consistent with apoptosis was detected in DNA harvested from amoebic liver lesions. These data suggest that neutrophils play an important role in the mechanisms of resistance to amoebic liver infection in mice. In addition, our histological analysis suggests that E. histolytica is capable of producing liver damage in the absence of inflammatory cells.

Animals↗

In vitro Entamoeba histolytica adhesion to human endothelium: a comparison using two strains of different virulence.

Extraintestinal dissemination of Entamoeba histolytica is frequently manifested by the life-threatening amebic liver abscess (ALA). The hepatic establishment of amebas implies invasion of blood vessels and contact with the endothelium. By means of a fluorescence-based quantitative adhesion assay, we assessed the binding to human endothelial cells of two E. histolytica strains of different virulence. The highly virulent strain (L-A) adhered substantially more strongly to unstimulated endothelium than the non-virulent one (BG3). Attachment of L-A was increased by treatment of endothelial cells with interleukin-1 beta (IL1 beta). Other proinflammatory cytokines such as interferon-gamma (IFN gamma) and tumor necrosis factor-alpha (TNF alpha) did not modify the spontaneous adhesion capacity of amebas. For purposes of comparison we also performed adhesion of the parasites to skin fibroblasts. Adhesion to this cell type was quite low (< 10%). Parasite virulence, differential adhesive capacity to endothelial cells, and modulation of the latter phenomenon by proinflammatory factors (IL1 beta) may influence the evolution and outcome of extraintestinal amebiasis, especially hepatic abscesses.

Animals↗

Active immunization in hamsters with live Entamoeba histolytica trophozoites of low virulence.

Live trophozoites of Entamoeba histolytica of low virulence (LV) were inoculated intraportally in hamsters. One week later they were challenged intrahepatically with highly virulent (HV) trophozoites of the same strain and sacrificed 1 week later. Significant protection manifested by the production of smaller lesions was observed in immunized animals. Antiamebic IgG levels were significantly higher in the immunized group. Histologically, livers of immunized animals presented small lesions containing foamy macrophages, epithelioid cells, fibroblasts and devoid of amebas. Lymphocyte and plasma cell infiltrates were seen periportally.

Animals↗

Early invasive intestinal amebiasis in Mongolian gerbils.

Mongolian gerbils were inoculated intracecally with E. histolytica trophozoites cultured monoxenically. During the first hours of interaction an increase in mucus production was observed. Microulcerative mucosal lesions appeared 24 to 72 h post-inoculation. Inflammatory infiltrate and edema of the lamina propria were associated with necrotic foci. At 96 h, the cecal mucosa was normal and live amebas were no longer detected. It is concluded that gerbils are useful as experimental models for studying the early stages of invasive intestinal amebiasis.

Animals↗

Morphological characterization of experimental amebic liver lesions in gerbils.

Gerbils are susceptible to amebic liver abscess (ALA) production under experimental conditions. However, little is known about the histopathological changes that occur during the evolution of the lesion. We analyzed microscopically the sequence of cellular events of ALA in gerbils inoculated intraportally or intrahepatically with E. histolytica. At early stages trophozoites were associated with different degrees of inflammatory reaction. Amebas were also observed in areas devoid of inflammatory cells. Damaged hepatocytes were either related or not to inflammatory reaction. At late stages, lysis of macrophages and epithelioid cells were seen in relation to necrotic tissue and trophozoites. We conclude that amebic liver necrosis in gerbils at early stages may result from lysis of inflammatory cells as shown previously by us in hamsters, but also by direct contact and lytic activity of amebas to hepatocytes. The late destruction and expansion of hepatic tissue necrosis is apparently associated with damage of macrophages and epithelioid cells.

Animals↗

Histological changes during healing of experimental amebic liver abscess treated with metronidazole.

Morphological changes during the healing of amebic liver abscess (ALA) in hamsters treated with metronidazole were studied. Animals with ALA of 4 days of evolution were treated orally with metronidazole (5 mg/100 g for 10 days). Liver samples were studied at different times from the beginning of treatment up to 22 days. The resolution of ALA was accompanied by chronic inflammatory reaction, increased number of foamy macrophages and gradual disappearance of the granulomas. Neoformed hepatocytes and blood vessels, and proliferation of biliary ducts were also observed. Foamy macrophages play an important role in the adequate healing of ALA.

Animals↗