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Biomedical subjects

A Pacheco

Publications and source records attributed to A Pacheco.

At least 37 records · Page 2Linked to original sources
PubMed1998

Eosinophilic lung disease associated with Candida albicans allergy.

A significant number of cases of chronic eosinophilic pneumonia remain idiopathic in spite of a comprehensive search of associated causes. This study reports a patient with a classical clinical presentation of chronic eosinophilic pneumonia and peripheral blood eosinophilia in whom selective sensitization to Candida albicans was demonstrated. This yeast was present in the bronchoalveolar lavage culture and specific serum immunoglobulin (Ig)E and IgG against C. albicans were found in the patient's serum. Levels of these specific immunoglobulins diminished with corticosteroid treatment and increased coinciding with a new outbreak of symptoms after lowering the dosage of corticosteroids. To the author's knowledge, this is the first case described of chronic eosinophilic pneumonia associated with sensitization to C. albicans. Evaluation of allergy to C. albicans should be performed in chronic eosinophilic pneumonia before labelling cases as idiopathic.

Adult↗
PubMed1997

Molecular basis of sulfite oxidase deficiency from the structure of sulfite oxidase.

The molybdenum-containing enzyme sulfite oxidase catalyzes the conversion of sulfite to sulfate, the terminal step in the oxidative degradation of cysteine and methionine. Deficiency of this enzyme in humans usually leads to major neurological abnormalities and early death. The crystal structure of chicken liver sulfite oxidase at 1.9 A resolution reveals that each monomer of the dimeric enzyme consists of three domains. At the active site, the Mo is penta-coordinated by three sulfur ligands, one oxo group, and one water/hydroxo. A sulfate molecule adjacent to the Mo identifies the substrate binding pocket. Four variants associated with sulfite oxidase deficiency have been identified: two mutations are near the sulfate binding site, while the other mutations occur within the domain mediating dimerization.

Amino Acid Sequence↗
PubMed1996

Herpes virus saimiri transformation of T cells in CD3 gamma immunodeficiency: phenotypic and functional characterization.

The characterization of T cell immunodeficiencies could in part be supported by using stable cell lines in which biochemical and molecular studies of the defect could be carried out thereby omitting frequent bleeding of patients. First attempts to obtain such cell lines included HTLV-I transformation and exogenous IL-2 administration, but both models have important disadvantages. Recently, a virus isolated from the squirrel monkey, Herpes virus saimiri (HVS), has been reported to have the ability to transform T cells. A stable IL-2-dependent HVS-transformed T cell line from a CD3 gamma deficient patient has been obtained; and this cell line displays both the phenotypic and the functional characteristics of the patient's lymphocytes. Moreover, the line down-modulates TCR/CD3 surface expression upon CD3 engagement, as do the patient's lymphocytes, showing that CD3 gamma and its phosphorylation are not necessary for TCR/CD3 internalization. In addition, the abnormal staining pattern of different anti-TCR/CD3 monoclonal antibodies is preserved in the HVS-patient line. Since HVS is capable of transforming CD3 gamma- T cells, the CD3 gamma chain does not seem to be involved in the HVS receptor process. The fact that it is not possible to obtain a CD8+ HVS line from the CD3 gamma- patient supports the existence of a functional anomaly in his scanty CD8+ peripheral lymphocytes. Thus, HVS transformation is a suitable model for T cell immunodeficiency studies and characterization. It may also be used in the future in cellular models for in vitro gene therapy trials.

CD3 Complex↗
PubMed1994

Primary T lymphocyte immunodeficiency associated with a selective impairment of CD2, CD3, CD43 (but not CD28)-mediated signal transduction.

A 2-year-old female with important signs of immune response failure against virus, bacteria, fungi and protozoa and no obvious humoral or lymphocyte phenotypical defect was studied. Both peripheral blood mononuclear cells and IL-2-dependent T cell lines derived from the patient showed a severe selective T cell activation impairment via CD2, CD3 and CD43; however, this defect was reversible with the addition of either IL-2, or phorbol myristate acetate (PMA) or anti-CD28 antibodies. Concordantly, the induction of IL-2 (and, in part, IL-3 and IL-4) messenger RNA was severely reduced in stimulated T cells, but that of other cytokines was either normal (IL-5) or only slightly diminished (interferon-gamma (IFN-gamma)). It is concluded that an activation T cell defect exists previous to protein kinase C (PKC) and between membrane receptors and the activation pathway of certain response genes encoding for interleukins involved in proliferation (i.e. IL-2, IL-3 and IL-4), but not of others (i.e. IL-5). The use of T cell lines from human T lymphocyte activation deficiencies allows dissection of T cell pathology and the corresponding physiological pathways. In the present description, there is an evident independence of the CD28 T cell activation pathway from those induced through CD2 or CD3, and the differential gene regulation of the different interleukins.

Antigens, CD↗
PubMed1994

Is sodium acetate dextran superior to sodium chloride dextran for small volume resuscitation from traumatic hemorrhagic shock?

Small volumes (4 mL/kg body weight (bw)) of hypertonic sodium chloride dextran effectively restore cardiac output and nutritional blood flow and increase arterial pressure in severe hemorrhagic shock. It has been suggested that the chloride anion be replaced with acetate to provide a solution that avoids the risk of hyperchloremia and has the advantage of supplying a buffering base to optimize hypertonic resuscitation. This study compares the effects of hypertonic sodium chloride dextran solution (7.2% NaCl/10% dextran 60 [NaCl-Dx]; n = 7) with sodium acetate dextran (10.4% Na-Ac/10% dextran 60 [NaAc-Dx]; n = 6) on hemodynamic, oxygen transport, and metabolic variables. Both solutions had the identical osmolality (2400 mOsmol/kg). Dogs (16.9 +/- 1.9 kg) were anesthetized and mechanically ventilated. Shock was induced by exteriorization of intestine and blood withdrawal (50% of blood volume) to maintain mean arterial blood pressure (MAP) at 40 mm Hg for 75 min. Thereafter, resuscitation was performed either with NaCl-Dx (4 mL/kg over 2 min) or NaAc-Dx (4 mL/kg over 4 min). During hypertonic resuscitation, there was a short-lasting decrease in MAP, which was more pronounced in the NaAc-Dx group (delta MAP -7.3 +/- 2.5 mm Hg). Cardiac index and oxygen consumption were normalized within 5 min after resuscitation with both solutions. In NaAc-Dx-treated animals, MAP remained at lower values as compared to NaCl-Dx-treated dogs at 5 and 30 min after resuscitation (52 +/- 3 vs 74 +/- 6, and 61 +/- 7 vs 79 +/- 12 mm Hg; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1993

A decrease in the estimated frequency of the extended HLA haplotype B18 CF130 DR3 DQw2 is common to non-insulin-dependent diabetes, juvenile rheumatoid arthritis, and Berger's disease.

Extended HLA haplotypes frequencies were estimated from the HLA, C2, Bf and C4 phenotypes of 74 patients with non-insulin-dependent diabetes (NIDD), 92 with juvenile rheumatoid arthritis (JRA), 44 with Berger's disease (BD), 83 with insulin-dependent diabetes (IDD), and 140 healthy controls. The extended HLA haplotype B18 CF130 DR3 DQw2, which is common (around 10% phenotype frequency) in healthy Spaniards and in other populations of paleo-North African origin, was found to be significantly less frequent in NIDD, JRA and BD, whereas its frequency was normal in IDD (although DR3 DQw2 haplotypes were increased in the latter disease). These data support the existence of a common HLA-linked pathogeneic mechanism in NIDD, JRA and BD, and point to a genetic difference between IDD and NIDD at the HLA level. This effect is readily detectable in our population because the uncommon BfF1 allele marks that haplotype instead of the more common BfS, which marks B8 CS01 DR3 DQw2 in other Caucasians. Our results support the hypothesis of strong selective pressures operating at the HLA level to preserve extended HLA haplotypes with advantageous gene sets from dilution by crossing-over. Imbalanced incomplete haplotypes may give rise to inappropriate T-cell repertoire selection in the thymus and/or antigen handling in the periphery, and be partly responsible for the pathogenesis of certain HLA-linked diseases (i.e. NIDD, JRA, and BD).

Alleles↗
PubMed1993

Selective disbalances of peripheral blood T lymphocyte subsets in human CD3 gamma deficiency.

The selection of T lymphocytes in the thymus and their activation upon the encounter with foreign antigens in the periphery require the aggregation and signals of the T cell receptor (TcR)/CD3 complex and several surface molecules termed coreceptors (notably CD4 or CD8 and CD45). The spatial arrangement and interactions of the different molecules in the resulting multimolecular recognition structure are mostly unknown. Here we report, from studies on a healthy human CD3 gamma deficiency, that the lack of the CD3 gamma component of the TcR/CD3 complex is associated with a long-term severe defect of peripheral blood CD4+ CD45RA+ and CD8+ lymphocytes, whereas CD4+CD45RO+, B and natural killer lymphocytes are unaffected. These results suggest that the CD3 gamma site of the TcR/CD3 complex is required for the peripheral representation of certain T cell types.

CD3 Complex↗
PubMed1993

Selective impairment of T lymphocyte activation through the T cell receptor/CD3 complex after cytomegalovirus infection.

Cytomegalovirus (CMV) infection is reported to cause transient immunosuppression in man. In this study we have analysed the effect of CMV on T lymphocyte function in 29 children diagnosed for acute CMV infection. Peripheral blood mononuclear cells (PBMC) obtained from the patients showed a significant specific impairment in their proliferative response to enterotoxins A and C1, to concanavalin A and to the anti-CD3 MoAb OKT3. The impaired responses were corrected with exogenous IL-2. In contrast, stimulation using phytohaemagglutinin, as well as activation signals delivered through the surface molecules CD26 or CD28, elicited normal proliferative responses in CMV PBMC. The results indicate that the T cell anergy associated with CMV infection is restricted to the T cell receptor/CD3 activation pathway.

Antigens, CD↗
PubMed1993

T lymphocyte signalling defects and immunodeficiency due to the lack of CD3 gamma.

A selective CD3 gamma defect, involving point mutations in both the paternal and the maternal genes, has been analyzed. The CD3 gamma defect affected two brothers of a four sibs family; one of them died at the age of 3 of a viral pneumonia with concomitant autoimmune features (Haemolytic anaemia and gut epithelial cell autoantibodies), whereas the other is still alive at the age of 10 with relatively mild infection episodes. In this work, the effects of the absence of the CD3 gamma chain in the structure and signal transduction of the T-cell receptor (TCR)/CD3 complex and in the selection and function of T lymphocytes were studied. The absence of CD3 gamma did not prevent the expression of certain amounts of TCR/CD3 complexes on the surface of T lymphocytes. This suggests the existence of at least two TCR/CD3 isoforms in T cells, either with or without CD3 gamma. A persistent low proportion of CD8+ T cells, not functional in vitro (they were unable to proliferate) and probably in vivo (associated to a lethal viral pneumonia), was observed. In contrast, the proportion of CD4+ T cells was not altered, and they were functional both in vitro (they showed a normal proliferation and a low, but detectable, increase of cytosolic Ca2+ in response to anti-TCR/CD3 stimuli, although the production of IL-2 was impaired) and in vitro (they normally helped B cells). These results show that the absence of CD3 gamma affects the selection and function of cytotoxic, but apparently not helper, T lymphocytes, although the possibility that the CD4+ T cells represent a specific subpopulation can not be ruled out. They also suggest that the interactions of the TCR/CD3 complex with its co-receptors during thymic selection and antigen recognition in the periphery may be asymmetrical, with CD8 interacting through CD3 gamma and, probably, CD4 through the homologous CD3 delta.

Autoimmunity↗
PubMed1992

Pleural effusion as first sign of extramedullary plasmacytoma.

A patient with mediastinal EP with extension to pleural spaces and subsequent pleural effusion is described. The finding of many plasma cells in pleural fluid led to diagnosis. Similar histologic findings such as multiple myeloma and immunoblastic lymphoma were ruled out by clinical approach and immunochemistry, respectively. This pleural effusion represents the first case described caused by EP.

Humans↗
PubMed1991

Community acquired pneumonia caused by Chlamydia pneumoniae strain TWAR in chronic cardiopulmonary disease in the elderly.

The role of Chlamydia pneumoniae in respiratory infections is controversial. Seroepidemiological studies in different countries have shown an incidence of around 50% of previous contact, whereas prospective studies only in the USA have detected 6-10% of C. pneumoniae in community acquired pneumonias; in a similar Swedish study no cases were detected. There have been no descriptions of this Chlamydia in Mediterranean countries. The acute antibody response indicative of recent infection is accepted if the microimmunofluorescence test shows a fourfold rise in antibody or a titer 1/6 or higher of the IgM fraction. Since the introduction of the microimmunofluorescence test in our hospital, we have detected 4 cases of pneumonia associated to TWAR antibody in a current study of 63 cases of community acquired pneumonias which required hospitalization. All 4 patients presented chronic cardiopulmonary diseases. These facts and additional seroepidemiological studies with a frequency of 53% of previous contact, show that C. pneumoniae has a nonrare etiology in Spain and could be an endemic condition.

Aged↗