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Biomedical subjects

V Tsutsumi

Publications and source records attributed to V Tsutsumi.

At least 19 recordsLinked to original sources
PubMed1992

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↗
PubMed1992

Scanning electron microscopy of erythrophagocytosis by Entamoeba histolytica trophozoites.

We analyzed by scanning electron microscopy (SEM) the sequence of erythrocyte ingestion by a virulent strain of Entamoeba histolytica trophozoites. Axenic cultures of amebas were placed in chamber plastic slides for 30 min. Human red blood cells (RBC) were added to the wells in a ratio of 1:100, ameba:erythrocytes. After different times of interaction, cells were fixed and processed for SEM. Erythrophagocytosis by E. histolytica is characterized by random suction of cells at early stages and polarization of the phagocytic event at one end of the parasite during later stages.

Animals↗
PubMed1992

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↗
PubMed1992

Model of intestinal amebiasis: structural and functional lesions to the rabbit colon mucosa by Entamoeba histolytica lysates.

Although the events occurring during the initial interaction of E. histolytica trophozoites with the mucosa of the large intestine probably determine the invasion by the parasites, an appropriate experimental model does not exist. To develop such a model we used full-thickness rabbit colon preparations (0.28 cm2) mounted in Ussing-type chambers. Untreated preparations had electrophysiological properties (potential difference, short-circuit current and electrical resistance) similar in magnitude and duration to those reported for stripped colonic mucosa. Exposure to E. histolytica trophozoite lysates for up to 80 min produced dose-dependent lesions in the colon, consisting of: (a) increased decay rates for potential difference, short-circuit current and transmural resistance, and (b) mucosal lesions involving vacuolation at the bases and shortening of epithelial cells, loss of intercellular junctions, destruction of microvilli, and necrosis of interglandular epithelial zones. The specificity and speed of the electrophysiologic effects and their correlation with the microscopic lesions suggest that this new model will help to understand the initial pathogenic events of intestinal amebiasis.

Animals↗
PubMed1992

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↗
PubMed1992

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↗
PubMed1991

Distribution of substance P and vasoactive intestinal peptide in the human liver: light and electron immunoperoxidase methods of observation.

The localization of substance P (SP) and vasoactive intestinal peptide (VIP) in 12 normal human liver tissues was examined by light and electron immunohistochemistry using immunoperoxidase methods. SP and VIP immunoreactive nerve fibers were observed around portal veins, bile ducts, and hepatic arteries in portal areas, along sinusoids and hepatocytes in hepatic lobules, and around central veins. More SP and VIP immunoreactive nerve fibers were present in the portal areas than in other regions. Moreover, SP and VIP containing nerve endings were localized close to myofibroblasts, Ito cells, fibroblasts and endothelial cells of blood vessels, and sinusoids. The results suggested that part of the innervation of the human liver may be related to the contraction and relaxation of the cells close to nerve endings, and to the regulation of hemodynamic processes by the neurotransmitters such as SP and VIP at the hepatic lobular level.

Adult↗
PubMed1990

[Experimental hepatic amebiasis: acute inflammation in the rat].

Rat livers inoculated intraportally with trophozoites of E. histolytica were studied by light and electron microscopy. At one hour post-inoculation, trophozoites were localized at the hepatic sinusoids without inflammatory reaction and only slight vascular congestion. From two hours post-inoculation, trophozoites were associated with small inflammatory foci distributed at random. At three to four hours, trophozoites showed signs of cellular damage. After eight hours, no parasites were seen and only some lymphoplasmocytic infiltration were detected. It is suggested that in the experimental hepatic amebic infection in the rat the acuta inflammatory reaction associated to trophozoites plays a role in the parasite rejection.

Animals↗
PubMed1990

[Experimental intestinal amebiasis: invasion and extension of the amebic lesion].

A morphological analysis of an experimental model of invasive intestinal amebiasis was carried out using the washed-closed cecal loop model in hamsters and guinea-pigs. By light microscopy, few amebic trophozoites adhered to the intestinal epithelium, whereas many associated to the mucus blanket. Some trophozoites attached to the interglandular epithelium, during the first 10 to 15 hours of interaction. Hereafter, the parasites destroyed gradually the epithelium and were associated with normal and lysed inflammatory cells. Some amebas have cell debris and erythrocytes in their cytoplasms. Typical amebic ulcer contained abundant trophozoites at the basolateral area. The results suggest that intestinal mucus and muscularis mucosa are temporal barriers to amebic invasion and extension of the ulcer. At the mucosal and submucosal levels, lysis of inflammatory cells produced by amebas seems to play an important role in the extension of the ulcer.

Animals↗
PubMed1990

[Role of macrophages and T-lymphocytes: resistance of guinea pigs to amebic liver infection].

The mechanisms of host resistance in hepatic amebiasis are poorly understood. Previous studies in guinea-pigs have shown that amebic liver infection is mild and cures spontaneously in approximately four days, in contrast to hamsters, where amebic liver infection progresses to coalescent abscesses that kill the animals in about one month. To determine the role of macrophages in the resistance of guinea-pigs to hepatic amebic infection, animals were treated with intraportal injection of Entamoeba histolytica, using the same route. Results showed that the amebic hepatic lesions are larger and require longer time to cure in the silica-treated group. This suggests that macrophages play a role in the resistance of the guinea-pig to amebic liver infection. The possible dependence of T lymphocytes in the resistance of guinea pigs to amebic hepatic infection was analyzed using Cyclosporin A. Results showed that resistance to E. histolytica liver infection is not related to circulating T lymphocytes. We conclude that the guinea-pig is a suitable experimental model for the study of natural host resistance mechanisms in hepatic amebiasis. Macrophages, but not T lymphocytes participate as an effective cellular immune response to eradicate amebic infection in the liver of guinea-pigs.

Animals↗
PubMed1989

Ultrastructure of experimental intestinal invasive amebiasis.

The morphological features of early intestinal ulcerations induced in rodents with axenic cultures of Entamoeba histolytica were studied by scanning and transmission electron microscopy. Amebas did not attach to the luminal surface of the mucosa except at interglandular regions, where parasites penetrated apparently through pseudopodial movement. Once in the lamina propria, trophozoites multiplied and destroyed mucosal components. Damage extended laterally through the mucosa, but progression to deeper layers of the intestinal wall was prevented by the muscularis mucosae, which acted as a partial barrier. This was eventually breached at focal points where amebas invaded the submucosa. Electron microscopy clearly showed the lysis of abundant polymorphonuclear neutrophil leukocytes (PMNs) by the amebas at the periphery of intestinal ulcerations as well as the lack of bacteria at these sites. This study demonstrates that recruitment and destruction of inflammatory cells following intestinal amebic invasion may take place in the absence of bacterial multiplication. The observations provide histological support to the hypothesis that lysis of PMNs by trophozoites participates in the genesis of amebic intestinal lesions.

Animals↗
PubMed1988

Inflammatory reaction in experimental hepatic amebiasis. An ultrastructural study.

One of the hallmarks of tissue necrosis produced by the human protozoan parasite Entamoeba histolytica, the causative agent of human amebiasis, appeared to be the lack of inflammatory reaction to the invading trophozoites. Recent evidence suggests, however, that inflammatory cells do appear during early stages of amebic destructive lesions and that they contribute to the establishment of foci of tissue necrosis in intestinal and liver lesions. The present analysis of the fine-structural changes that take place during early stages of amebic liver abscesses induced in hamsters after the intraportal inoculation of axenic amebas has shown that large numbers of polymorphonuclear leukocytes (PMNs) are recruited around invading amebas. These leukocytes lyse as a consequence of contact-mediated damage induced by the trophozoites. Amebas were also capable of ingesting apparently intact PMNs. Macrophages and eosinophils were also recruited at the foci of inflammation. At all times examined, trophozoites of Entamoeba histolytica survived in spite of being in close contact with PMNs or degranulating eosinophils. The ultrastructural observations have also shown the lack of direct contact between amebas and liver parenchymal cells during the initial stages of the focal liver necrosis induced by the parasite, therefore supporting the view that hepatic damage may be effected indirectly through lysis of inflammatory cells. The results also provide a basis for the understanding of the induction of experimental protective immunity against invasive amebiasis, a process which seems to be mostly dependent on cellular mechanisms.

Amebiasis↗
PubMed1985

Purification and characterization of GP-55, a protein associated with actin-based cytoplasmic gels derived from brain tissue.

Incubation of rat brain cytoplasmic extracts results in the formation of three-dimensional gels that can be collapsed by low-speed centrifugation. Electrophoresis in polyacrylamide gels indicate that these cytoplasmic gels are composed of actin and several associated proteins. Among the latter we have identified a component with an apparent molecular mass of 55,000 daltons. The results of two-dimensional electrophoresis, peptide mapping, and in vivo labeling experiments with [35S]methionine, indicate that the 55-kDa protein is composed of two different gene products we have named alpha and beta; a third polypeptide, named beta', probably derives from the beta polypeptide as a result of some posttranslational modification(s). These three polypeptides, which have the same molecular weight but different isoelectric points, are present in a rather pure preparation of the 55-kDa protein, obtained from cytoplasmic gels by ion-exchange chromatography. In vitro, purified 55-kDa protein interacts in a specific manner with F-actin, as shown by viscosimetry and electron microscopy, leading to the formation of a complex network of cross-linked microfilament bundles. The results of immunofluorescence experiments indicate that the 55-kDa protein is located intracellularly in structures belonging to the Golgi apparatus, and that it is not only present in every type of rat cell tested but also in primary cultures of chick embryo neurons. Based on its intracellular location, we have named the 55-kDa protein as Golgi Protein-55 (GP-55).

Actins↗
PubMed1985

Intestinal invasive amebiasis: an experimental model in rodents using axenic or monoxenic strains of Entamoeba histolytica.

A new experimental model for the production of early stages of invasive intestinal amebiasis in hamsters or guinea pigs with axenic or monoxenic cultures of Entamoeba histolytica of the HM1:IMSS strain is reported. The model is called the washed-closed cecal loop, because it involves the washing out of the cecum contents of conventionally raised animals and the formation of a closed loop, into which amebas are inoculated. Colonization occurred in all inoculated animals. After 48 hr, macroscopic ulcerations of the cecal mucosa were found in approximately one-half (5/12) of the animals inoculated with axenic amebas and in more than two-thirds (10/12) of those inoculated with monoxenic parasites. The amebic nature of the mucosal ulcerations was confirmed by light and transmission electron microscopy, as well as by scanning electron microscopy (SEM) of fractured samples of cecal mucosa. SEM provided a rapid and reliable technique to assess both the extent and the nature of the lesions. This model is particularly useful for the study of the pathogenesis of early intestinal lesions produced by virulent amebas, and may also be applied to experimental studies on the immunology of invasive intestinal amebiasis.

Amebiasis↗
PubMed1979

Adrenocortical function in hypophysectomized dogs with parotid gland transplants in direct contact with the basal hypothalamus.

Adrenocortical activity was studied in three groups of dogs: control-normal, hypophysectomized (hypox), and dogs with a piece of parotid gland grafted into the sella turcica immediately after removal of the whole hypophysis (hypox + graft). Cortisol plasma level (Fk) was estimated by the competitive protein binding method. The mean base-line Fk for 21 normal dogs was 0.8 +/- 0.1 microgram/dl; for 12 hypox dogs 0.03 +/- 0.01 microgram/dl, and for hypox + graft dogs 0.5 +/- 0.2 microgram/dl. After mild or severe stresses the normal and hypox + graft dogs showed an increment in Fk; hypox dogs showed no change. Adrenal glands of hypox dogs revealed striking diminution in fasciculata and reticularis layers, whereas hypox + graft dogs approached normal. Light microscopy studies of the parotid gland graft showed signs of cellular differentiation. Groups of proliferating cells forming follicular structures were present mainly in the part of the parotid tissue closely associated to third ventricle presenting different staining affinities.

Adrenal Cortex↗
PubMed1975

Granular cell tumor (myoblastoma) of the orbit.

An 8-year-old white boy had a tumor in the left orbit with clinical manifestations of muscular impairment, exophthalmos, and reduced visual acuity. Five months after exenteration of the orbit the boy was healthy without tumor recurrence. Based on our observations with electron, light, and phase microscopy, and histochemical studies, we conclude that this tumor is benign, of histiocytic origin, and we propose the term granular cell histiocytoma be used to describe this entity.

Cell Nucleolus↗