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Biomedical subjects

R Campos-Rodríguez

Publications and source records attributed to R Campos-Rodríguez.

At least 19 recordsLinked to original sources
PubMed2003

Human amoebic hepatic abscess: in situ interactions between trophozoites, macrophages, neutrophils and T cells.

Amoebic liver abscesses (ALA) are the most frequent and severe extraintestinal clinical presentations of amoebiasis. During the early establishment of amoebae in the liver parenchyma, as well as during the extension of the tissue necrosis, parasites interact with the parenchymal liver cells and, as a consequence of these interactions, hepatocytes can be destroyed and host immune cells can become activated. However, little is known about the nature of these interactions in the liver or about the factors involved in the local immune response. In this investigation we studied the localization of Entamoeba histolytica trophozoites, TCD4+, TCD8+ cells, CD68+ macrophages and CD15+ neutrophils in human ALA using immunohistochemical techniques. Trophozoites were found close to undamaged hepatocytes in both lysed and non-lysed areas with either sparse or abundant inflammatory infiltrate. CD8+ cells were more abundant than CD4+ T cells. CD 68+ macrophages and CD15+ neutrophils were also detected, suggesting that neutrophils, macrophages and T cells might be related to the local host immune mechanisms in ALA. We also found that E. histolytica possesses proteins recognized by antibodies raised against inducible nitric oxide synthase.

Animals↗
PubMed2002

Entamoeba histolytica: immunohistochemical study of hepatic amoebiasis in mouse. Neutrophils and nitric oxide as possible factors of resistance.

Studies in mice have not rendered conclusive data on cell and humoral factors to support the resistance of this rodent to Entamoeba histolytica infection. In Balb/c and C3H/HeJ mice inoculated with live or fixed trophozoites, we studied the evolution of the hepatic lesion, the kinetics of inflammatory cells, and the participation of some humoral factors in the development of the hepatic amoebic lesion. From the first hour, amoebae were surrounded by neutrophils containing inducible nitric oxide synthase (iNOS); macrophages also expressing iNOS appeared lately, whereas NK cells were not part of the inflammatory infiltrates. On the fourth day, neutrophils, macrophages, T and B lymphocytes, plasma cells, and some NK cells limited the lesions and anti-amoeba antibodies appeared when most parasites had been eliminated. Therefore, the resistance of the mice to E. histolytica probably lies in non-specific immune responses, among which the activation of neutrophils and the production of nitric oxide (NO) may be important amoebicide factors.

Animals↗
PubMed2002

Early interactions of Entamoeba histolytica trophozoites with parenchymal and inflammatory cells in the hamster liver: an immunocytochemical study.

We studied the early in situ interactions of live and fixed Entamoeba histolytica trophozoites with hamster hepatic parenchymal and inflammatory cells using immunoperoxidase and immunoelectronmicroscopy. Close contact between trophozoites and endothelial cells and the diffusion of amoebic molecules from trophozoites towards nearby endothelial cells and distant hepatocytes were observed. The inflammatory cells around the amoebae and the remnants of parenchymal cells and hepatocytes located close to the lesion had a positive stain for amoebic molecules. In the amoebae, at the ultrastructural level, molecules were attached to the membranes and inside the vesicles. These molecules were apparently released into the space formed between the parasite and the endothelial cells. The endothelial cells and the nearby and distant hepatocytes captured amoebic molecules, and later they became necrotic. Contrarily, when fixed amoebae were inoculated, amoebic molecules were captured by endothelial cells and polymorphonuclear (PMN) leukocytes, but neither suffered any damage. In this work, we are presenting evidence clearly showing that some molecules of the amoeba can diffuse away long distances causing cytotoxic effects and even necrosis on hepatic cells of hamster liver without the need of the trophozoite being in close contact with the target cells. They also may promote lytic or proinflammatory effects by inducing the secretion of enzymes or cytokines in other nonparenchymal cells, like PMN leukocytes and endothelial cells. Our results suggest that the accepted mechanisms of cytotoxicity by amoebae are not exclusively restricted to the following sequence: adhesion, phagocytosis, and necrosis.

Animals↗
PubMed2001

Entamoeba histolytica: production of nitric oxide and in situ activity of NADPH diaphorase in amebic liver abscess of hamsters.

Entamoeba histolytica trophozoites were inoculated into the liver of hamsters and serum nitrate/nitrite levels [expressed as nitric oxide (NO) production] were determined at different times during amebic liver abscess (ALA) development. We also tested the effects of NO synthase (NOS) inhibitors such as N(G)-nitro-L-arginine methyl ester (L-NAME), aminoguanidine, and dexamethasone during ALA production. Since NOS activity has been correlated with expression of reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) in tissues, we performed histochemistry studies to determine the activity of the latter in livers infected with E. histolytica trophozoites. Production of NO in serum was directly proportional to the size of ALAs, and NOS inhibitors caused low levels of NO and smaller ALAs. Our data suggest that NO does not have any lytic effect on E. histolytica trophozoites and is therefore incapable of providing protection against the amebic liver infection. In addition, NADPHd activity was detected histochemically in hepatocytes and inflammatory cells associated with focal necrosis containing trophozoites. The positive reactivity observed in these parasites may be attributable to a close biochemical similarity of NADPHd to the NADPH:flavin oxidoreductase described in E. histolytica by other investigators.

Animals↗
PubMed2000

Interaction of antibodies with Entamoeba histolytica trophozoites from experimental amebic liver abscess: an immunocytochemical study.

Using immunocytochemical techniques, we studied the interaction of antibodies with Entamoeba histolytica trophozoites present during the development of amebic liver abscess. Hamsters were intrahepatically inoculated with HM1-IMSS axenic amebas and sacrificed at different days post-inoculation. IgG of rabbit anti-E. histolytica and IgG of rabbit anti-IgG of hamster were used, both labeled with peroxidase. With the rabbit anti-E. histolytica, all trophozoites present in hepatic lesions from 1-7 days post-inoculation were highly labeled. The IgG of rabbit anti-IgG of hamster intensively stained only those trophozoites present in lesions from 1-2 days post-inoculation. From day 3, the intensity and number of labeled trophozoites decreased progressively. The results suggest that the interaction between the amebas and the IgG of hamster is non-specific during the first 2 days. The absence of labeling in the chronic stages could be due to changes in the membrane antigens of the parasite or to alterations in the bloodstream around necrosis. Also, the anti-E. histolytica antibodies produced in the serum during the development of the hepatic disease are apparently incapable of reaching and interacting with the trophozoites present on the liver abscess. This can explain in part why antibodies do not have an important role in the defense of the host.

Animals↗
PubMed2000

Immunoblot analysis of IgA antibodies to Naegleria fowleri in human saliva and serum.

The objective of this study was to evaluate the secretory IgA (SIgA) antibody response to Naegleria fowleri (Nf) in individuals living in a parasite endemic area. Saliva and serum samples were obtained from both healthy subjects and patients suffering from a respiratory illness (chronic bronchitis or rhinitis) and were analyzed by immunoblot assay. SIgA from the patients' samples recognized more intensely a greater number of Nf proteins than did SIgA from the healthy control group. The proteins more frequently recognized were those with a molecular weight of 171, 107, 102, 62, 50, 46, and 10 kDa. Some IgA antibodies recognized proteins from Nf and Entamoeba histolytica (Eh) of similar molecular weight. These results suggest that some of those antibodies could have been elicited by a previous intestinal infection with Eh. Through the common mucosal immune system the IgA B-cells activated by Eh antigens can be disseminated to all the mucosae, including the nasal mucosa. SIgA antibodies recognizing Nf proteins, induced either by specific immunization or by cross-reaction, could participate in the resistance to the infection, probably by inhibiting the adherence of Nf trophozoites to the nasal mucosa.

Amebiasis↗
PubMed1998

Entamoeba histolytica: liver invasion and abscess production by intraperitoneal inoculation of trophozoites in hamsters, Mesocricetus auratus.

Intraperitoneal inoculation of axenically cultured Entamoeba histolytica trophozoites constitutes an easy to perform, highly reproducible procedure for inducing amebic liver abscesses in hamsters. Efficiency in abscess production (95% of infected animals after 1 week) was similar to data reported using direct intrahepatic or intraportal inoculation. The morphological sequence of infection shows that amebas in the peritoneal cavity initially produce a large exudate constituted mainly of acute inflammatory cells. These cells form a rim of polymorphonuclear leukocytes surrounding the amebas, which adhere to the trophozoite and can sometimes be observed polarized to one end of the parasite, suggesting capping of surface receptors. Early stages are also characterized by the production of distant inflammatory reactions in the hepatic portal spaces. At 6 h postintraperitoneal inoculation, larger foci of inflammatory reactions surrounding amebas are developed in the peritoneum, extending to and damaging the liver surface membranes as well as the serosa of other internal organs. Thereafter, tissue damage progresses deeper into the liver parenchyma, and a few days later, coalescing granulomas and large necrotic areas are observed in the liver tissue. Based on the present morphological time-sequence study, we suggest that inflammatory cells associated with E. histolytica trophozoites play an important role in commencing the damage of liver sheaths and producing the subsequent parenchymal lesions. The simplicity and reliability of this model are important factors to consider when large numbers of experimentally induced amebic liver abscesses are needed.

Animals↗
PubMed1997

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↗
PubMed1997

Human amebic liver abscess: expression of intercellular adhesion molecules 1 and 2 and of von Willebrand factor in endothelial cells.

Liver invasion by amebas with production of amebic liver abscess (ALA) is the most common extraintestinal lesion produced by the protozoan parasite Entamoeba histolytica. This hepatic damage is characterized by the presence of extensive tissue necrosis. However, little is known about the parasite and host factors involved in the process of tissue damage. During the early establishment of amebas in the liver parenchyma as well as during the extension of the tissue necrosis, parasites interact with sinusoidal endothelial cells. As a consequence of ameba-endothelial cell interactions, the latter can be activated and express proinflammatory factors that could be related to tissue destruction. We studied by immunohistochemistry the localization of antigenic molecules of E. histolytica trophozoites and of molecules such as intercellular adhesion molecule 1 (ICAM-1), ICAM-2, and von willebrand factor in activated endothelial cells of human ALA, which could be related to the pathophysiological mechanisms of tissue destruction in amebiasis.

Adolescent↗
PubMed1992

Sex differences in systemic and local immune responses to Entamoeba histolytica after intraperitoneal and rectal immunization in Balb/c mice.

The antibody responses against Entamoeba histolytica in Peyer's patches and spleen after rectal, intraperitoneal and intragastric immunization with glutaraldehyde-fixed amebas (GFA) was compared between male and female mice by the use of a spot forming cell (SFC) assay. We found that female mice elicit significant higher anti-amebic SFC responses than male mice, in both spleen and Peyer's patches after rectal and intraperitoneal stimulation, whereas by intragastric route females show higher responses than males in spleen but not in Peyer's patches.

Animals↗
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

Kinetics of the anti-amebic antibody producing cells response in Peyer's patches and spleen after both local and systemic stimulation in Balb/c mice.

The kinetics of the anti-amebic antibody producing cell (APC) response was analyzed by a spot forming cell (SFC) assay, after a single dose of glutaraldehyde fixed amebas (GFA) by intragastric, rectal and intraperitoneal routes. It was found that mice elicited both local and systemic immune responses in Peyer's patches and spleen, by either local or systemic stimulation. The analysis of the isotype of the anti-amebic APC in mice given four times the GFA by the mentioned routes revealed that mice produced anti-amebic APC of the three major isotypes in both spleen and Peyer's patches.

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

[Prevalence of dental caries and rampant caries in a preschool population].

The results from a study on prevalence of ordinary dental caries and rampant caries in a children population are presented. The study was carried out at Dentistry Out patient Service in the Children Hospital "San Juan de Aragón" of the Federal District Department. The DMF index was obtained and its was proposed another one, in order to classify the different degrees of rampant caries in function of dental damage. An interview was applied to the fathers of the children of the study group in order to determinate hygiene oral habits, eating and familiar antecedents that could influence in the process of the ordinary and rampant caries and to compare between them. Serum and saliva were analyzed to determinate levels of albumin and IgM, IgG and IgA; there were also others factors tested that could indicate caries development.

Child↗