Dr. Antonio Condino-Neto

@article{pmid16181054,

title = {The effect of IFN-gamma and TNF-alpha on the NADPH oxidase system of human colostrum macrophages, blood monocytes, and THP-1 cells},

author = {Ana Carolina Almeida and Jussara Rehder and Silvana Dalgè Severino and José Martins-Filho and Peter E Newburger and Antonio Condino-Neto},

doi = {10.1089/jir.2005.25.540},

issn = {1079-9907},

year  = {2005},

date = {2005-09-01},

journal = {J Interferon Cytokine Res},

volume = {25},

number = {9},

pages = {540--546},

abstract = {The aim of this work was to analyze the effect of Interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) on NADPH oxidase activity and gp91-phox gene expression in human colostrum macrophages (CM), peripheral blood monocytes (PBM), and myelomonocytic THP-1 cells. We also investigated the effect of IFN-gamma on the release of TNF-alpha by these cells. Our results show that under basal culture conditions, CM release more superoxide than PBM and THP-1 cells (p < 0.05). The addition of IFN-gamma, alone or in combination with TNF-alpha, increased spontaneous superoxide release by PBM and THP-1 cells (p < 0.05) and increased phorbol myristate acetate (PMA)-stimulated superoxide release by CM, PBM, and THP-1 cells (p < 0.05). The NADPH oxidase activity of THP-1 cells consistently remained lower than that of CM or PBM, despite a dramatic response to IFN-gamma and TNF-alpha. Under basal conditions, gp91-phox gene expression was significantly higher in CM and PBM compared with THP-1 cells (p < 0.05). The addition of IFN-gamma alone or in combination with TNF-alpha caused a dramatic increase in gp91-phox gene expression in THP-1 cells (p < 0.05) but not in CM or PBM. Under basal conditions or in the presence of IFN-gamma, CM released more TNF-alpha than PBM or THP-1 cells (p < 0.05). In addition, PBM released more TNF-gamma than THP-1 cells (p < 0.05). IFN-gamma did not significantly augment the release of TNF-alpha by these cells (p > 0.05). Thus, IFN-gamma and TNF-alpha induced equivalent gp91-phox gene expression in THP-1 cells compared with CM or PBM but did not bring about equivalent NADPH oxidase activity. TNF-alpha release was higher in more mature cells. This partial divergence of gp91- phox gene expression, NADPH oxidase activity, and TNF-alpha release is probably a consequence of different events of myeloid cell biology and relates at least in part to cell differentiation state.},

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pubstate = {published},

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}

@article{pmid15787870,

title = {Mites in dust samples from mattress surfaces from single beds or cribs in the south Brazilian city of Londrina},

author = {Dagoberto Ribeiro da Silva and Raquel Soares Binotti and Cleide Moreira da Silva and Celso Henrique de Oliveira and Antônio Condino-Neto and Eduardo Mello de Capitani},

doi = {10.1111/j.1399-3038.2005.00210.x},

issn = {0905-6157},

year  = {2005},

date = {2005-03-01},

journal = {Pediatr Allergy Immunol},

volume = {16},

number = {2},

pages = {132--136},

abstract = {The aim of this study was to investigate the mite fauna in mattresses dust samples from cribs or beds in the south Brazilian city of Londrina, State of Parana. A total of 133 dust samples from upper and lower mattress surfaces, and bed frames were aspirated once from 38 dwellings (18 cribs and 21 beds), and one day nursery (six cribs). A total of 758 mite bodies were counted in slides: 233 (30.7%) from cribs and 525 (69.3%) from beds (p<0.001). House dust mites--mainly Dermatophagoides pteronyssinus, represented 72% and 84% of total mite count in crib and bed dust samples, respectively. The mean HDM body concentration in crib or bed slides were, respectively, 289.9+/-136.7 and 875.0+/-183.6 mites/g. Statistical analysis showed a significantly higher mite bodies count on lower mattress surface compared with upper surface in bed samples only (p=0.025). Data herein show that cribs like mattress have sufficient mite bodies to cause sensitization to humans. The use of mattress covers for cribs and beds should be encouraged in order to avoid allergens exposure.},

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pubstate = {published},

tppubtype = {article}

}

@article{pmid15517074,

title = {Superoxide release and cellular gluthatione peroxidase activity in leukocytes from children with persistent asthma},

author = {L E Marçal and J Rehder and P E Newburger and A Condino-Neto},

doi = {10.1590/s0100-879x2004001100003},

issn = {0100-879X},

year  = {2004},

date = {2004-11-01},

journal = {Braz J Med Biol Res},

volume = {37},

number = {11},

pages = {1607--1613},

abstract = {Asthma is an inflammatory condition characterized by the involvement of several mediators, including reactive oxygen species. The aim of the present study was to investigate the superoxide release and cellular glutathione peroxidase (cGPx) activity in peripheral blood granulocytes and monocytes from children and adolescents with atopic asthma. Forty-four patients were selected and classified as having intermittent or persistent asthma (mild, moderate or severe). The spontaneous or phorbol myristate acetate (PMA, 30 nM)-induced superoxide release by granulocytes and monocytes was determined at 0, 5, 15, and 25 min. cGPx activity was assayed spectrophotometrically. The spontaneous superoxide release by granulocytes from patients with mild (N = 15), moderate (N = 12) or severe (N = 6) asthma was higher at 25 min compared to healthy individuals (N = 28, P < 0.05, Duncan test). The PMA-induced superoxide release by granulocytes from patients with moderate (N = 12) or severe (N = 6) asthma was higher at 15 and 25 min compared to healthy individuals (N = 28, P < 0.05 in both times of incubation, Duncan test). The spontaneous or PMA-induced superoxide release by monocytes from asthmatic patients was similar to healthy individuals (P > 0.05 in all times of incubation, Duncan test). cGPx activity of granulocytes and monocytes from patients with persistent asthma (N = 20) was also similar to healthy individuals (N = 10, P > 0.05, Kruskal-Wallis test). We conclude that, under specific circumstances, granulocytes from children with persistent asthma present a higher respiratory burst activity compared to healthy individuals. These findings indicate a risk of oxidative stress, phagocyte auto-oxidation, and the subsequent release of intracellular toxic oxidants and enzymes, leading to additional inflammation and lung damage in asthmatic children.},

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pubstate = {published},

tppubtype = {article}

}

@article{pmid15234534,

title = {Hyperresponsiveness of neutrophils from gp 91phox deficient patients to lipopolysaccharide and serum amyloid A},

author = {Elaine Hatanaka and Beatriz Tavares Costa Carvalho and Antônio Condino-Neto and Ana Campa},

doi = {10.1016/j.imlet.2004.04.016},

issn = {0165-2478},

year  = {2004},

date = {2004-06-01},

journal = {Immunol Lett},

volume = {94},

number = {1-2},

pages = {43--46},

abstract = {We demonstrate here that neutrophils from chronic granulomatous disease (CGD) patients release larger amounts of interleukin-8 (IL-8) and tumor necrosis factor alpha (TNF-alpha) than neutrophils from control subjects. Incremental cytokine production was observed under both basal and stimulated conditions in neutrophils from two CGD (gp 91phox) patients. The basal production of IL-8 was over seven-fold greater in CGD patients. The two samples assayed showed 3- and 10-fold increases in TNF-alpha. Basically, the same magnitude of increment was observed in lypopolysaccharide (LPS) and serum amyloid A protein (SAA)-stimulated cells. We also found that the levels of SAA and IL-8 were higher in the serum of CGD patients than the levels found in the serum of healthy donors. The increased responsiveness of neutrophils from CGD patients may be closely related with a deficiency in the assembly of the nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase enzyme system, or it may be due to a frequent inflammatory condition in these patients. In the latter case, the increased serum levels of systemic inflammatory factors, among them SAA, would contribute to the sustained accumulation and activation of phagocytes. Whatever the origin, the excessive production of cytokines may lead to inappropriate activation and tissue injury and even to increased susceptibility to invasive microorganisms, impairing the quality life of CGD patients.},

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pubstate = {published},

tppubtype = {article}

}

@article{pmid15107922,

title = {The use of reverse transcription-PCR for the diagnosis of X-linked chronic granulomatous disease},

author = {P Agudelo-Flórez and J A López and J Redher and M M S Carneiro-Sampaio and B T Costa-Carvalho and A S Grumach and A Condino-Neto},

doi = {10.1590/s0100-879x2004000500001},

issn = {0100-879X},

year  = {2004},

date = {2004-05-01},

journal = {Braz J Med Biol Res},

volume = {37},

number = {5},

pages = {625--634},

abstract = {Chronic granulomatous disease (CGD) is an inherited disorder of the innate immune system characterized by a defective oxidative burst of phagocytes and subsequent impairment of their microbicidal activity. Mutations in one of the NADPH-oxidase components affect gene expression or function of this system, leading to the phenotype of CGD. Defects in gp91-phox lead to X-linked CGD, responsible for approximately 70% of CGD cases. Investigation of the highly heterogeneous genotype of CGD patients includes mutation analysis, Northern blot or Western blot assays according to the particular case. The aim of the present study was to use reverse transcription (RT)-PCR for the analysis of molecular defects responsible for X-linked CGD in eight Brazilian patients and to assess its potential for broader application to molecular screening in CGD. Total RNA was prepared from Epstein B virus-transformed B-lymphocytes and reverse transcribed using random hexamers. The resulting cDNA was PCR-amplified by specific and overlapping pairs of primers designed to amplify three regions of the gp91-phox gene: exons 1-5, 3-9, and 7-13. This strategy detected defective gp91-phox expression in seven patients. The RT-PCR results matched clinical history, biochemical data (nitroblue tetrazolium or superoxide release assay) and available mutation analysis in four cases. In three additional cases, RT-PCR results matched clinical history and biochemical data. In another case, RT-PCR was normal despite a clinical history compatible with CGD and defective respiratory burst. We conclude that this new application of RT-PCR analysis--a simple, economical and rapid method--was appropriate for screening molecular defects in 7 of 8 X-linked CGD patients.},

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pubstate = {published},

tppubtype = {article}

}

@article{pmid14978696,

title = {Association of glucose-6-phosphate dehydrogenase deficiency and X-linked chronic granulomatous disease in a child with anemia and recurrent infections},

author = {Piedad Agudelo-Flórez and Beatriz T Costa-Carvalho and Juan Alvaro López and Jussara Redher and Peter E Newburger and Sara Teresinha Olalla-Saad and Antonio Condino-Neto},

doi = {10.1002/ajh.10477},

issn = {0361-8609},

year  = {2004},

date = {2004-03-01},

journal = {Am J Hematol},

volume = {75},

number = {3},

pages = {151--156},

abstract = {Patients with severe leukocyte G6PD deficiency may present with impairment of NADPH oxidase activity and a history of recurrent infections, mimicking the phenotype of chronic granulomatous disease. We report herein a child with recurrent infections who initially received the diagnosis of G6PD deficiency. His erythrocyte G6PD activity was reduced: 1.8 U/g Hb (normal: 12.1 +/- 2.1 U/g Hb). Further studies revealed that G6PD activity in neutrophils, mononuclear leukocytes, and Epstein-Barr virus-transformed B-lymphocytes from the proband was similar to healthy controls. Molecular studies showed that the G6PD deficiency was due a 202 G-->A mutation, the A- variant common in African ethnic groups. The proband also exhibited severely impaired respiratory burst activity, as observed in X-linked CGD. Sequence analysis of genomic DNA showed a 264 G-->A substitution at the 3' splice junction of gp91-phox exon 3. The cDNA sequence showed a deletion of gp91-phox exon 3, giving rise to an unstable or nonfunctional mutant gp91-phox and to the phenotype of X-linked CGD. We propose that clinicians treating a patient with G6PD deficiency during a severe infection episode consider the possibility of temporary or permanent impairment of the phagocytes' microbicidal activity and the eventual association of G6PD deficiency and chronic granulomatous disease.},

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pubstate = {published},

tppubtype = {article}

}

@article{pmid15505740,

title = {[Autosomal chronic granulomatous disease: case report and mutation analysis of two Brazilian siblings]},

author = {Carolina Prando-Andrade and Piedad Agudelo-Florez and Juan A Lopez and Maria Aparecida de Souza Paiva and Beatriz T Costa-Carvalho and Antônio Condino-Neto},

issn = {0021-7557},

year  = {2004},

date = {2004-01-01},

journal = {J Pediatr (Rio J)},

volume = {80},

number = {5},

pages = {425--428},

abstract = {OBJECTIVE: To report the case of two siblings with chronic granulomatous disease. Chronic granulomatous disease is a primary immunodeficiency disorder characterized by abnormal microbicidal activity. Mutations in the p47-phox gene (NCF-1) are present in about 30% of the patients with chronic granulomatous disease; this group presents a better prognosis and later onset of recurrent infections as compared with the X-linked variant, present in about 56% of patients.nnDESCRIPTION: Case 1 is a female presenting repeat infections since age 10, starting with impetigo followed by severe pneumonia six months later. The severity of the lung infection associated with liver abscess and the patient's resistance to treatment prompted laboratory investigation for immunodeficiency. The results of the nitroblue tetrazolium and superoxide release tests were consistent with a diagnosis of chronic granulomatous disease. The parents and siblings were assessed, revealing the presence of granulomatous disease in a brother (Case 2). He also presented repeat infections with impetigo at age 10, followed by pneumonia six months later, however in a non severe form. Single-strand conformational polymorphism analysis detected abnormal electrophoretic mobility of exon 2 of the NCF-1 gene. Sequence DNA analysis revealed a dinucleotide GT deletion in exon 2.nnCOMMENTS: It is important to evaluate the relatives of chronic granulomatous disease patients, even in the absence of typical clinical signs. Defining the mutation and its correlation with phenotype is important to provide appropriate genetic counseling and clinical prognosis.},

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pubstate = {published},

tppubtype = {article}

}

@article{pmid14769150,

title = {The effect of IFN-gamma and TNF-alpha on the eosinophilic differentiation and NADPH oxidase activation of human HL-60 clone 15 cells},

author = {Juan A Lopez and Peter E Newburger and Antonio Condino-Neto},

doi = {10.1089/107999003772084851},

issn = {1079-9907},

year  = {2003},

date = {2003-12-01},

journal = {J Interferon Cytokine Res},

volume = {23},

number = {12},

pages = {737--744},

abstract = {The aim of this study was to investigate the effect of interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) on NADPH oxidase activity and gp91-phox gene expression in HL-60 clone 15 cells as they differentiate along the eosinophilic lineage. The results were compared to the eosoniphilic inducers interleukin-5 (IL-5) and butyric acid. IFN-gamma (100 U/ml) and TNF-alpha (1000 U/ml) or IL-5 (200 pM) caused a significant increase in the expression of the eosinophil peroxidase (EPO) and the major basic protein (MBP) genes. Similar results were observed when the cells were cultured with 0.5 mM butyric acid for 5 days. IFN-gamma (100 U/ml) and TNF-alpha (1000 U/ml) also caused a significant increase in superoxide release by HL-60 clone 15 cells after 2 days compared with control or with butyric acid-induced cells. After 5 days, these cytokines and butyric acid induced an even stronger release of superoxide. HL-60 clone 15 cells cultured with IFN-gamma and TNF-alpha for 2 days showed a significant increase in gp91-phox gene expression. We conclude that IFN-gamma and TNF-alpha are sufficient to induce the differentiation of HL-60 clone 15 cells to the eosinophilic lineage and to upregulate gp91-phox gene expression and activity of the NADPH oxidase system.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid12358341,

title = {Are immunoglobulin E levels associated with early wheezing? A prospective study in Brazilian infants},

author = {N Lopez and S de Barros-Mazon and M Marluce dos Santos Vilela and A Condino Neto and J D Ribeiro},

doi = {10.1183/09031936.02.00219302},

issn = {0903-1936},

year  = {2002},

date = {2002-09-01},

journal = {Eur Respir J},

volume = {20},

number = {3},

pages = {640--645},

abstract = {The relationship between wheezing or asthma and serum immunoglobulin (Ig)E levels in early life is unclear. The aim of this study was to follow-up the IgE immune response in infants that did, or did not, develop recurrent wheezing during their first year of life. One-hundred and two randomised term neonates were included, in which IgE levels were quantified in cord blood samples, at 3, 6, 9 and 12 months of age. Specific IgE levels for food and inhalant allergens and the skin-prick test for inhalant allergens were also assessed at 6 and 12 months. During clinical follow-up, 32 (31%) infants presented with two or more wheezing episodes, while 70 (69%) had no wheezing. Total IgE levels were significantly higher up to 12 months in wheezing infants when compared to nonwheezing group. At 12 months, the specific IgE levels to cow's milk, egg white and mites were higher in infants with recurrent wheezing. There was no influence of family history for atopy on IgE levels. The skin-prick tests were positive in 14% and 23% in wheezing infants at 6 and 12 months, respectively. These results indicate an early allergic sensitisation in wheezing infants, suggesting an altered immunoregulatory T-cell role in immunoglobulin E production.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid14647844,

title = {[Effects of cisapride and chest physical therapy on the gastroesophageal reflux of wheezing babies based on scintigraphy]},

author = {M A Ribeiro and M L Cunha and E C Etchebehere and E E Camargo and J D Ribeiro and A Condino-Neto},

doi = {10.2223/jped.281},

issn = {1678-4782},

year  = {2001},

date = {2001-01-01},

journal = {J Pediatr (Rio J)},

volume = {77},

number = {5},

pages = {393--400},

abstract = {OBJECTIVE: To evaluate the effect of cisapride and chest physical therapy on the gastroesophageal reflux of wheezing babies. METHODS: We prospectively assessed the presence of technetium ((99)Tc) in the upper, middle, and lower esophagus of 25 wheezing babies (13 with GERD and 12 without GERD) using scintigraphy. Both groups underwent clinical investigation, including laboratory, X-ray and scintigraphy tests, for the etiology of the wheezing baby syndrome (WBS) and GERD. Expiratory Flow Acceleration (EFA) was performed before and after treatment with cisapride. The total time of GER episodes was accounted for each portion of the esophagus during scintigraphy and during EFA. RESULTS: Cisapride significantly reduced the total reflux time in the upper esophagus (P<0.05), but showed no influence during EFA. After cisapride therapy, EFA increased the total reflux time in the upper and medium esophagus; however, no statistical significance was found. Infants with GERD presented a shorter total reflux time in the distal esophagus (P<0.05) during EFA. After cisapride treatment, no statistical significance was found. Infants without GERD also presented reduced total reflux time in the distal esophagus during EFA (P<0.05). Those with GERD had increased total reflux time in the distal esophagus (P<0.05) before and after cisapride treatment during EFA and scintigraphy. CONCLUSIONS: Cisapride was effective in reducing the total reflux time, mainly in the upper esophagus. EFA apparently increased the number of episodes of GER, without achieving statistical significance. Further studies are necessary to investigate the effects of chest physical therapy according to body positions.},

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}