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Biomedical subjects

M M Teixeira

Publications and source records attributed to M M Teixeira.

At least 19 recordsLinked to original sources
PubMed2006

Eotaxin-2 in sputum cell culture to evaluate asthma inflammation.

The aim of the present study was to elucidate whether the culture of cells recovered from induced sputum may represent a suitable model to evaluate cytokine and chemokine production by airway inflammatory cells. Sputum induction was performed in 21 normal subjects and 30 asthmatic patients. A total of 21 out of the 30 asthmatic patients were taking inhaled corticosteroids, while the remaining nine were steroid-naive asthmatics. The steroid-naive group was evaluated before and after a 14-day treatment with oral prednisone (40 mg.day(-1)). The supernatant of lysed and centrifuged sputum and the supernatant of sputum cell culture were analysed. Tumour necrosis factor-alpha, interleukin (IL)-8 (CXCL8), IL-1beta, IL-13 and eotaxin-2 (CCL24) concentrations were determined by specific ELISA. Eotaxin-2 production by cell culture was higher in the asthma group (131+/-108 pg.mL(-1)) than in the control group (36+/-41 pg.mL(-1)) and treatment with oral corticosteroids eliminated this difference. In addition, reduction of eotaxin-2 levels by corticosteroid treatment was greater in cell culture (81.3% reduction) than in sputum (26.4%). There was correlation between the decrease in eotaxin-2 production and the decrease in blood eosinophil number and between eotaxin-2 and eosinophils in sputum. Eotaxin-2 may play an important role in asthma and the response to corticosteroid treatment suggests that analysis of sputum cell culture is relevant as an inflammatory parameter.

Administration, Inhalation↗
PubMed2006

Chemokines in the cerebrospinal fluid of patients with active and stable relapsing-remitting multiple sclerosis.

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the human central nervous system. Although its etiology is unknown, the accumulation and activation of mononuclear cells in the central nervous system are crucial to its pathogenesis. Chemokines have been proposed to play a major role in the recruitment and activation of leukocytes in inflammatory sites. They are divided into subfamilies on the basis of the location of conserved cysteine residues. We determined the levels of some CC and CXC chemokines in the cerebrospinal fluid (CSF) of 23 relapsing-remitting MS patients under interferon-ss-1a therapy and 16 control subjects using ELISA. MS patients were categorized as having active or stable disease. CXCL10 was significantly increased in the CSF of active MS patients (mean +/- SEM, 369.5 +/- 69.3 pg/mL) when compared with controls (178.5 +/- 29.1 pg/mL, P < 0.05). CSF levels of CCL2 were significantly lower in active MS (144.7 +/- 14.4 pg/mL) than in controls (237.1 +/- 16.4 pg/mL, P < 0.01). There was no difference in the concentration of CCL2 and CXCL10 between patients with stable MS and controls. CCL5 was not detectable in the CSF of most patients or controls. The qualitative and quantitative differences of chemokines in CSF during relapses of MS suggest that they may be useful as a marker of disease activity and of the mechanisms involved in the pathogenesis of the disease.

Adjuvants, Immunologic↗
PubMed2006

Concentrations of CXCL8, CXCL9 and sTNFR1 in plasma of patients with pulmonary tuberculosis undergoing treatment.

BACKGROUND: Chemokines are a class of cytokines with chemotactic properties shown to be induced by M. tuberculosis or its antigens in vitro and in experimental infection in vivo. A few studies have also demonstrated the expression of chemokines in clinical samples of patients with active tuberculosis (TB). In the present work, we measured the concentration of chemokines in plasma samples of HIV-negative patients with pulmonary tuberculosis at different stages of chemotherapy. For comparison, we also evaluated the levels of sTNFR1 and TNF-alpha. METHODS: Cytokines and chemokines were measured by ELISA in healthy individuals and patients with active pulmonary TB at different stages of treatment. RESULTS: The concentrations of CXCL8, CXCL9 and sTNFR1 were elevated in patients with active pulmonary TB but returned to background levels at 4-6 months of chemotherapy. The concentration of CCL11 was elevated in patients with active pulmonary tuberculosis when compared to control and remained elevated throughout the specific therapy. There was no difference in the plasma concentration of CCL2 and CXCL10 between pulmonary TB patients and control subjects. CONCLUSION: Measurement of the CXCL8, CXCL9 and sTNFR1 may be useful to assess response to treatment in pulmonary TB patients.

Cytokines↗
PubMed2006

Levels of serum chemokines discriminate clinical myelopathy associated with human T lymphotropic virus type 1 (HTLV-1)/tropical spastic paraparesis (HAM/TSP) disease from HTLV-1 carrier state.

Approximately 5% of people infected with human T lymphotropic virus type 1 (HTLV-1) develop clinical myelopathy or tropical spastic paraparesis (HAM/TSP) that is associated with high-levels of Th1 cytokines, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha. Chemokines are known to induce cytokine secretion and direct the trafficking of immune cells to sites of disease. The present study measured serum chemokines correlated with autonomously released IFN-gamma in cell cultures. HTLV-1 infection was defined by enzyme-linked immunosorbent assay (ELISA) and confirmed by Western blot. Subjects included HTLV-1 carriers (n = 56), patients with HAM/TSP (n = 31) and healthy HTLV-1 seronegative volunteer controls (n = 20). Serum chemokines and IFN-gamma autonomously released by mononuclear cells in culture were quantified by ELISA. Compared to HTLV-1 carriers, serum chemokines in HAM/TSP patients showed significantly increased levels of CXCL9 and CXCL10, significantly diminished levels of CCL2 and similar amounts of CCL11 and CCL24. In contrast, CCL11 and CCL24 were significantly lower in serum of HAM/TSP patients than either control. IFN-gamma was positively correlated with CXCL9 and CXCL10 when HAM/TSP and HTLV-1 carriers were used as a combined group. However, despite a large proportion of HTLV-1 carriers having high IFN-gamma levels, these chemokines were not increased in carriers. This study showed that high levels of CXCL9 and CXCL10 in the systemic circulation and low serum CCL2 levels are features of HAM/TSP. HTLV-1 infection and Tax and/or additional viral encoded factor-mediated pathological processes triggering T cell activation with autogenous IFN-gamma release are probably involved in regulating chemokine release.

Biomarkers↗
PubMed2006

Serum and cerebral spinal fluid levels of chemokines and Th2 cytokines in Schistosoma mansoni myeloradiculopathy.

Schistosomal myeloradiculopathy (SMR) is the most common neurological form of Schistosoma mansoni infection. In this study we investigated the expression of chemokines and Th2 cytokines in serum and cerebral spinal fluid (CSF) of SMR patients. SMR patients presented increased serum levels of CCL11/eotaxin and CCL24/eotaxin-2 when compared to controls. SMR patients also had higher levels of IL-13 in CSF. Thus, SMR patients present enhancement of both IL-13 and CCR3 acting chemokines, both of which may facilitate the expression of a Th2 response and Th2-dependent damage to the spinal cord. As this cytokine is responsible for promoting Th2 responses, this finding is in accordance to the view that Th2 cells are important in the immunological process against the S. mansoni.

Adolescent↗
PubMed2006

Effect of the treatment with methylprednisolone on the cerebrospinal fluid and serum levels of CCL2 and CXCL10 chemokines in patients with active multiple sclerosis.

BACKGROUND: Several experimental and human studies suggest that the chemokines CCL2 and CXCL10 may play a role in the pathogenesis of multiple sclerosis (MS). Here, we evaluated the effect of intravenous methylprednisolone (IVMP) therapy on the levels of CCL2 and CXCL10 in the cerebrospinal fluid (CSF) and serum of patients with active MS. METHODS: Serum and CSF samples were obtained from 14 patients with active relapsing-remitting MS (age +/- SD years, 37.0 +/- 8.1; M/F, 6/8) and age- and gender-matched control subjects. All patients were submitted to IVMP treatment (500 mg daily for 5 days). Blood and CSF sampling were performed at admission, i.e. before treatment (day 0), at the end of the treatment (day 6) and 30 days after treatment (day 30). The clinical status of MS patients was also assessed. CCL2 and CXCL10 were measured by enzyme-linked immunosorbent assay. RESULTS: Multiple sclerosis patients had lower CCL2 and higher CXCL10 in CSF when compared with control subjetcs. After treatment with methylprednisolone, MS patients showed clinical improvement and the CSF concentrations of CCL2 and CXCL10 modified toward normal values. CONCLUSIONS: The clinical improvement of active MS following the treatment with methylprednisolone was associated with the modification of CSF levels of CCL2 and CXCL10, suggesting that these chemokines may be useful markers of response to treatment and relapses in MS patients.

Adult↗
PubMed2005

Angiogenesis and inflammation in skeletal muscle in response to ascites tumor in mice.

This study addresses the interaction between Ehrlich ascites tumor and skeletal abdominal muscle, presenting quantitative analysis of ascites-induced angiogenesis and inflammation in this tissue of mice bearing-tumor. Time-dependent changes in the muscle (cellular activity, angiogenesis, inflammation and cytokines production) were assessed by morphometric, functional, and biochemical parameters at days 1, 4 and 8 after i.p. inoculation of Ehrlich tumor cells (2.5 x 10(7)). The number of cells stained with AgNOR technique (argyrophilic nucleolar organizer region) in the muscle, together with MTS assay used as markers of cellular activity increased progressively in parallel with the out flow rate of sodium fluorescein (blood flow index), hemoglobin content (vascular index) and VEGF production. Likewise, the inflammatory process in the muscle, as assessed by myeloperoxidase (MPO) and n-acethylglucosaminidase (NAG) activities and the levels of the chemokines, keratinocyte-derived chemokine (CXC1-3/KC) and macrophage-chemoattractant protein (CCL2/MCP-1) increased with tumor development. The combination of techniques used to describe angiogenesis and inflammation in a muscle model system has proved to be suited for quantitative measurements of microvascular changes and cellular infiltration occurring in the abdominal muscle wall of ascites-bearing mice. This study holds potential for investigating events and mechanisms associated with skeletal muscle response to neoplasic stimulus.

Animals↗
PubMed2005

Concentration of CCL11, CXCL8 and TNF-alpha in sputum and plasma of patients undergoing asthma or chronic obstructive pulmonary disease exacerbation.

Asthma and chronic obstructive pulmonary disease (COPD) are common respiratory illnesses characterized by chronic inflammation of the airways. The characterization of induced or spontaneously produced sputum is a useful technique to assess airway inflammation. In the present study, we compared the concentrations of CCL2, CCL11, CXCL8, and tumor necrosis factor-alpha (TNF-alpha) in plasma and induced sputum of patients with severe asthma or COPD and correlated the levels of these mediators with inflammatory cells in sputum. Asthmatic patients had elevated levels of eosinophils (40.1 +/- 6.24%) in sputum whereas neutrophils (63.3 +/- 4.66%) predominated in COPD patients. The levels of the chemokine CCL11 were markedly increased in sputum (708.7 +/- 330.7 pg/ml) and plasma (716.6 +/- 162.2 pg/ml) of asthmatic patients and correlated with the percentage of eosinophils in induced sputum. The concentrations of CXCL8 (817.0 +/- 105.2 pg/ml) and TNF-alpha (308.8 +/- 96.1 pg/ml) were higher in sputum of COPD patients and correlated with the percentage of neutrophils in induced sputum. There was also an increase in the concentrations of CXCL8 (43.2 +/- 6.8 pg/ml) in sputum of asthmatic patients. These results validate that sputum is a suitable method to assess chemokines and cytokines associated with asthma and COPD. Moreover, the mechanisms involved in the synthesis of CCL11 and CXCL8/TNF-alpha would be helpful to better understand the inflammatory profile associated with asthma and COPD, respectively.

Adult↗
PubMed2005

CC-chemokine receptors: a potential therapeutic target for Trypanosoma cruzi-elicited myocarditis.

The comprehension of the pathogenesis of Trypanosoma cruzi-elicited myocarditis is crucial to delineate new therapeutic strategies aiming to ameliorate the inflammation that leads to heart dysfunction, without hampering parasite control. The augmented expression of CCL5/RANTES and CCL3/MIP-1alpha, and their receptor CCR5, in the heart of T. cruzi-infected mice suggests a role for CC-chemokines and their receptors in the pathogenesis of T. cruzi-elicited myocarditis. Herein, we discuss our recent results using a CC-chemokine receptor inhibitor (Met-RANTES), showing the participation of CC-chemokines in T. cruzi infection and unraveling CC-chemokine receptors as an attractive therapeutic target for further evaluation in Chagas disease.

Animals↗
PubMed2005

Impaired inflammatory angiogenesis, but not leukocyte influx, in mice lacking TNFR1.

The majority of biological responses classically attributed to tumor necrosis factor alpha (TNF-alpha) is mediated by p55 receptor (TNFR1). Here, we aimed to clarify the biological role of TNFR1-mediated signals in an in vivo inflammatory angiogenesis model. Polyester-polyurethane sponges, used as a framework for tissue growth, were implanted in C57Bl/6 mice. These implants were collected at days 1, 7, and 14 post-implant for enzyme-linked immunosorbent assay or at days 7 and 14 for hemoglobin, myeloperoxidase, and N-acetylglucosaminidase measurements, used as indexes for angiogenesis, neutrophil, and macrophage accumulation, respectively. In TNFR1-deficient C57Bl/6 mice, there was a significant decrease in sponge vascularization but not in late inflammatory cell influx. It is interesting that levels of vascular endothelial growth factor were significantly lower in TNFR1-deficient than in wild-type mice at days 1 and 7. Levels of angiogenic chemokines, CC chemokine ligand 2/murine homologue of monocyte chemoattractant protein-1 and CXC chemokine ligand 1-3/keratinocyte-derived chemokine, were significantly lower in TNFR1-deficient mice at days 1 and 7 after implantation, respectively. These observations suggest that TNFR1-mediated signals have a critical role in sponge-induced angiogenesis, possibly by influencing the effector state of inflammatory cells and hence, modulating the angiogenic molecular network.

Acetylglucosaminidase↗
PubMed2004

A model of chronic IgE-mediated food allergy in ovalbumin-sensitized mice.

Food allergy is most frequently the result of IgE-mediated hypersensitivity reactions. Here, we describe a chronic model in which some of the intestinal and systemic consequences of continuous egg white solution ingestion by ovalbumin-sensitized eight-week-old BALB/c mice, 6 animals per group, of both sexes, were investigated. There was a 20% loss of body weight that began one week after antigen exposure and persisted throughout the experiment (3 weeks). The sensitization procedure induced the production of anti-ovalbumin IgG1 and IgE, which were enhanced by oral antigen exposure (129% for IgG1 and 164% for IgE, compared to sensitization values). Intestinal changes were determined by jejunum edema at 6 h (45% Evans blue extravasation) and by a significant eosinophil infiltration with a peak at 48 h. By day 21 of continuous antigen exposure, histological findings were mild, with mast cell hyperplasia (100%) and increased mucus production (483%). Altogether, our data clearly demonstrate that, although immune stimulation was persistently occurring in response to continuous oral antigen exposure, regulatory mechanisms were occurring in the intestinal mucosa, preventing overt pathology. The experimental model described here reproduces the clinical and pathological changes of mild chronic food allergy and may be useful for mechanistic studies of this common clinical condition.

Animals↗
PubMed2004

Inhibition of inflammatory angiogenesis by distant subcutaneous tumor in mice.

We investigated angiogenesis, inflammatory cells accumulation and endogenous production of cytokines in sponge implants of tumor-bearing mice. Seven days after inoculation of Ehrlich tumor cells (2.5 x 10(6)), sponge discs were implanted subcutaneously in the dorsa of mice to induce the formation of fibrovascular tissue. The implants of tumor-bearing and non tumor-bearing animals were assessed for neovascularization and leukocyte accumulation, together with levels of relevant cytokines, vascular endothelial growth factor VEGF), tumor necrosis factor alpha (TNF-alpha), CXCL1-3/KC and CCL2/JE. In the implants of tumor-bearing animals angiogenesis (assessed by hemoglobin content and VEGF levels in the implants) and leukocyte accumulation (assessed by myeloperoxidase -MPO- and N- acetylglucosaminidase-NAG-enzyme activities) were all significantly less than those in the implants of non tumor-bearing animals. Although the chemokine CXCL1-3/KC was lower in the implants of tumor-bearing animals, the chemokine CCL2/JE was increased in this group. The production of TNF-alpha in the implants was not modified by the presence of the subcutaneous tumor. The combination of the methodologies used in this study has provided a novel approach to investigate the interaction between two distinct proliferating tissues that share common features (angiogenesis, cell recruitment, inflammation) and has shown that the predominant inhibitory effect of a tumor mass over repair process is associated with altered cytokine production.

Angiogenesis Inhibitors↗
PubMed2004

PTX3 function as an opsonin for the dectin-1-dependent internalization of zymosan by macrophages.

Pentraxin 3 (PTX3) is a tumor necrosis factor and interleukin-1beta-stimulated gene that encodes a long PTX with proinflammatory activity. Here, we show that peritoneal macrophages derived from PTX3 transgenic (Tg) mice express higher levels of PTX3 mRNA than macrophages from wild-type (WT) mice, at basal level as well as upon stimulation with zymosan (Zy). Macrophages from Tg mice also showed improved opsonin-independent phagocytosis of Zy particles and the yeast form of the fungus Paracoccidioides brasiliensis. In the case of P. brasiliensis, an enhanced microbicidal activity accompanied by higher production of nitric oxide was also observed in macrophages from Tg mice. Using fluorescein-activated cell sorter analysis and reverse transcriptase-polymerase chain reaction, we demonstrated that basal level of Toll-like receptor-6 and Zy-induced dectin-1 expression was slightly but consistently higher in macrophages from Tg mice than in macrophages from WT mice. Recombinant (r)PTX3 protein binds to Zy particles as well as to yeast cells of P. brasiliensis and addition of rPTX3, to a culture of WT-derived macrophages containing Zy leads to an increase in the phagocytic index, which parallels that of Tg-derived macrophages, demonstrating the opsonin-like activity of PTX3. It is important that blockade of dectin-1 receptor inhibited the phagocytosis of Zy particles by WT and PTX3 Tg macrophages, pointing out the relevant role of dectin-1 as the main receptor involved in Zy uptake. Our results provide evidence for a role of PTX3 as an important component of the innate-immune response and as part of the host mechanisms that control fungal recognition and phagocytosis.

Animals↗
PubMed2004

Production and in vivo effects of chemokines CXCL1-3/KC and CCL2/JE in a model of inflammatory angiogenesis in mice.

OBJECTIVE: Using the murine sponge model, we investigated the temporal relationship between angiogenesis, leukocyte accumulation and endogenous generation of the pro-inflammatory chemokines CXCL1-3/KC and CCL2/JE. Furthermore, the effects of exogenous administration of these chemokines were studied. METHODS: Angiogenesis in the implants was assessed by measuring the hemoglobin content (vascular index) and leukocyte accumulation quantified by evaluating MPO and NAG enzyme activities. RESULTS: A progressive increase in hemoglobin content and in enzymatic activities was observed during the whole period. The levels of CXCL1-3/KC and CCL2/JE in the implants peaked at days 7 and 1, respectively. Exogenous administration of CXCL1-3/KC (100 ng/day intra-implant) applied at days 1-3 resulted in increased neovascularization and macrophage accumulation. Intra-implant injections of CCL2/JE (100 ng/day) also resulted in increased angiogenesis and macrophage accumulation. CONCLUSIONS: These results demonstrated that the chemokines, CXCL1-3/KC and CCL2/JE, are generated within the sponge compartment and that neovascularization and inflammatory cells influx can be modulated by exogenous administration of the chemokines.

Acetylglucosaminidase↗
PubMed2003

[District allocation and utilization of health care services in Pau da Lima, Salvador, Bahia, Brazil].

This cross-sectional study is aimed at the identification of patterns in the utilization of health care services in Pau da Lima, a neighborhood in the city of Salvador, Bahia. In 1992, a household survey was carried out with 384 families selected through a random cluster sampling design. In each household, the family head or a surrogate informant was asked to answer a questionnaire about their use of any type of health care in the last month. From the total of 1,887 individuals, 236 reported at least one visit to health facilities during the referent period This means an estimated prevalence of health services utilization of 12.5%. With regard to the type of services, 25.9% of all visits were made to public sector facilities. Attendants were mainly women (73.7%) from 15 to 29 years of age. The main reason reported for the choice of the health facility was availability (63.7%), and the major reason for seeking health care was disease-related conditions (75.7%), rather than preventive procedures. These findings may result from the still unfinished process of distritalização(district allocation of services), which is evident in the lack of health services' infrastructure or coverage, as well as in persistent organizational problems. These issues may lead the population living in the respective district to seek health care outside the assigned catchment area. The authors discuss these findings in the context of the expansion of the private sector in the health area and the financial collapse of the public budget in Brazil.

English Abstract↗
PubMed2002

Mechanisms underlying the structural alterations of the rat submandibular gland induced by Tityus serrulatus tityustoxin.

As the mechanisms underlying the structural changes induced in rat submandibular glands by Tityus serrulatus tityustoxin have not been reported, the present study was undertaken to investigate the participation of adrenergic and muscarinic cholinergic receptors in these alterations. Most of the stimulatory effects of the toxin are observed in the secretory cells of the acini and granular convoluted tubules (GCT). We evaluated the ability of the toxin to induce morphological changes in acinar and GCT cells after adrenoreceptor and cholino receptor blockage. The influence of tityustoxin-induced adrenal discharge on the acinar and GCT cells was also investigated after bilateral adrenalectomy. We show that the intense cytoplasmic vacuolation of the acinar cells induced by tityustoxin was prevented by prazosin (alpha(1) adenoreceptor blockade) and atropine (muscarinic cholinoreceptor blockade). The decrease of GCT cell granules following tityustoxin injection was completely blocked by prasozin and partially by propranolol. These results indicate that acinar vacuolation, degranulation of GCT cells, reduction of GCT diameter and height of its epithelium depends on tityustoxin induced adrenergic and cholinergic mechanisms. In contrast, tityustoxin induced acinar cell degranulation was not modified by atropine, prasozin or propranolol (beta(1)-beta(2) adenoreceptor blockade). Thus, acinar degranulation seems to be due to a direct action of tityustoxin on of the rat submandibular glands. The degranulation of the GCT cells and the acinar vacuolation was also prevented by bilateral adrenalectomy, suggesting that these effects are mostly due to catecholamines released from the adrenal glands.

Adrenalectomy↗
PubMed2002

Role of the platelet-activating factor (PAF) receptor during pulmonary infection with gram negative bacteria.

The lipid mediator PAF plays an important role in the phagocytosis of particles, including bacteria, and consequent production of pro-inflammatory cytokines, such as TNF-alpha and IL-8. Using a PAF receptor antagonist (UK-74,505) and PAF receptor knock-out mice, we have investigated the relevance of PAF for the inflammatory changes and lethality after pulmonary infection with the gram-negative bacteria Klebsiella pneumoniae in mice. At an inoculum of 3 x 10(6) bacteria, there was marked pulmonary (bronchoalveolar lavage and lung) neutrophilia that started early (2.5 h after infection) and peaked at 48 h. All animals were dead by day 4 of infection. The chemokine KC and the pro-inflammatory cytokine TNF-alpha increased rapidly and persisted for 48 h in the lungs. Pretreatment with UK-74,505 (30 mg kg(-1) per day, p.o.) had no significant effects on the number of infiltrating neutrophils in BAL fluid or lung tissue, as assessed by histology and measuring myeloperoxidase, or on the concentrations of KC. In contrast, concentrations of TNF-alpha and the number of bacteria inside neutrophils were significantly diminished. In order to support a role for the PAF during K. pneumoniae infection, experiments were also carried out in PAFR-deficient mice. In the latter animals, lethality occurred earlier than in wild-type controls. This was associated with greater number of bacteria in lung tissue and diminished percentage of neutrophils containing bacteria in their cytoplasm. Our results suggest that PAF, acting on its receptor, plays a protective role during infection with K. pneumoniae in mice.

Animals↗