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1.
J Viral Hepat ; 13(12): 821-7, 2006 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-17109681

RESUMO

The alpha-defensin genes promoter regions contain a putative nuclear factors of activated T cells (NFAT)-binding site and it is known that hepatitis C virus (HCV) core protein activates the interleukin (IL)-2 gene transcription through the NFAT pathway. The aims of this study were to investigate if HCV affects the alpha-defensin expression in peripheral human mononuclear cells (PBMCs) and to evaluate the existence of a correlation between alpha-defensins and liver damage in patients with chronic hepatitis C. Ninety patients with chronic hepatitis C, 30 with chronic hepatitis B and 25 healthy controls were enrolled. Alpha-defensins were identified and quantified in PBMCs by mass spectrometry, enzyme-linked immunosorbent assay, antibacterial activity and mRNA levels. PBMCs from three patients and controls were stimulated with HCV core protein, hepatitis B virus core antigen and the alpha-defensin mRNAs level was quantified. We found that HCV core protein activates in vitro the alpha-defensin transcription. Alpha-defensin levels in patients with chronic hepatitis C (mean +/- SD = 1.103 +/- 0.765 ng/10(6) cells), chronic hepatitis B (0.53 +/- 0.15) and healthy controls (0.217 +/- 0.09) resulted significantly different (P < 0.001). In patients with chronic hepatitis C, the alpha-defensin levels and antibacterial activity correlate with the liver fibrosis. Our data suggest that HCV induces alpha-defensin expression. The high linear correlation of alpha-defensin levels with advancing fibrosis makes the measure of these peptides a reliable marker to evaluate fibrosis stage.


Assuntos
Anti-Infecciosos/imunologia , Hepatite C Crônica/imunologia , Leucócitos Mononucleares/imunologia , alfa-Defensinas/sangue , Adulto , Anti-Infecciosos/metabolismo , Feminino , Expressão Gênica , Hepatite C Crônica/sangue , Hepatite C Crônica/patologia , Hepatite C Crônica/virologia , Humanos , Cirrose Hepática/sangue , Cirrose Hepática/imunologia , Cirrose Hepática/virologia , Masculino , Pessoa de Meia-Idade , Regiões Promotoras Genéticas , RNA Mensageiro/biossíntese , RNA Mensageiro/genética , alfa-Defensinas/biossíntese , alfa-Defensinas/genética , alfa-Defensinas/imunologia
2.
Parasitology ; 118 ( Pt 4): 335-8, 1999 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-10340322

RESUMO

The C57BL6 strain of mice is highly susceptible to Plasmodium berghei sporozoite infections and consequently requires repeated immunizations with irradiated sporozoites to obtain protective immunity. After a live sporozoite challenge in the immunized hosts, hepatic-stage parasites found in the liver after 48 h are of different sizes--small schizonts corresponding to blocked forms (derived from irradiated sporozoites), and schizonts of intermediate size (derived from live sporozoites). Large schizonts corresponding to mature hepatic forms are found only in unimmunized but challenged C57BL6 mice. Using monoclonal and polyclonal antibodies directed to liver-stage parasites, different patterns of binding reactivity to the above forms are observed. More than 20% of the irradiated sporozoites transform into blocked forms after immunization and persist in the liver. Upon sporozoite challenge in such immunized animals the rate of transformation of sporozoites into hepatic parasites is less than 2%. These observations shed light on the fate of live sporozoite development in irradiated sporozoite-immunized C57BL6 mice.


Assuntos
Antígenos de Protozoários/imunologia , Imunização , Fígado/parasitologia , Malária/parasitologia , Plasmodium berghei/crescimento & desenvolvimento , Plasmodium berghei/imunologia , Animais , Anopheles/parasitologia , Anticorpos Antiprotozoários/imunologia , Feminino , Malária/prevenção & controle , Camundongos , Camundongos Endogâmicos C57BL , Plasmodium berghei/efeitos da radiação , Proteínas de Protozoários/imunologia
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