Biomedical subjects

B M Tavares-Murta

Publications and source records attributed to B M Tavares-Murta.

6 recordsLinked to original sources

PubMed2006

Neutrophil function in severe sepsis.

Sepsis and septic shock continue to be a major cause of morbidity and mortality in critically ill patients. During the onset of sepsis, several inflammatory mediators, including cytokines, chemokines and nitric oxide are released systemically and mediate most of the pathophysiological events present in sepsis and septic shock, such as cardiovascular dysfunction and target-organ lesions. Polymorphonuclear leukocytes are critical effector cells during the inflammatory process and their migration to the infection focus is extremely important for the local control of bacterial growth and consequently for the prevention of bacterial dissemination. In experimental models and in human sepsis a profound failure of neutrophil migration to the infection focus is observed. It seems that the failure of neutrophil migration is dependent on toll-like receptor 4 (TLR4) and mediated by cytokines and chemokines, which induce the production of nitric oxide that inhibits neutrophil adhesion to venular endothelium and also the neutrophil chemotactic ability.

Animals↗

PubMed2004

Ultrasonographic criteria and tumor marker assay are good procedures for the diagnosis of ovarian neoplasia in preselected outpatients.

PURPOSE OF INVESTIGATION: To identify parameters for the diagnosis of ovarian neoplasia using ultrasonography (US) and serum tumor marker (TM: CA125, CA19.9, CA15.3, AFP, CEA and estradiol) assay. METHODS: Prospective study which included 373 women with increased ovarian volume (> 18 cm3 in premenopause and > 8 cm3 in postmenopause). US criteria (> or = 1) for surgery were: persistent (> 4 months) or increased cyst, cysts with > 1 thick septum or > or = 2 thin septa, cyst diameter > or = 7 cm, vegetation, calcification or cystic predominance (> 50%), solid tumor (> 50%). Doppler with a resistance index (RI) < 0.4 was considered abnormal. RESULTS: Laparotomy was performed in 164 (44%) patients with 66 (40.2%) benign neoplasias and 19 (11.6%) malignant cases (73.6% at Stage I or II). Two hundred and nine patients were maintained on clinical follow-up. The sensitivity for neoplasia and malignant neoplasia was, respectively, for RI: 17 and 63.6 and RI plus TM: 53.1 and 90.9. CONCLUSION: Ultrasound criteria and TM assay were indicated for the diagnosis of ovarian neoplasia.

Adolescent↗

PubMed2001

Nitric oxide mediates the inhibition of neutrophil migration induced by systemic administration of LPS.

To investigate the role of NO in the inhibition of neutrophil migration by circulating endotoxin, mice were pretreated with NO synthase inhibitors or with a free radical scavenger (D-penicillamine), before intravenous LPS injection. LPS dose-dependently inhibited the thioglycollate-induced neutrophil migration into the peritoneal cavities. Aminoguanidine, a selective inducible NO synthase inhibitor, abolished the inhibition of neutrophil migration and the increase in serum nitrate levels induced by a nonlethal dose of LPS. During lethal endotoxemia aminoguanidine partially abolished the neutrophil migration inhibition. Additionally, D-penicillamine prevented the inhibition of neutrophil migration caused by LPS. However, Nitro-L-Arginine, a selective constitutive NO synthase inhibitor, did not prevent neutrophil migration inhibition. Aminoguanidine treatment did not affect the systemic increased levels of TNF-alpha, IL-1beta, and IL-10, suggesting that NO is the final mediator involved in the inhibition of neutrophil migration. Our results suggest that NO released by the inducible NO synthase mediates the inhibition of neutrophil migration mediated by circulating LPS.

Animals↗

PubMed1998

The intravenous administration of tumor necrosis factor alpha, interleukin 8 and macrophage-derived neutrophil chemotactic factor inhibits neutrophil migration by stimulating nitric oxide production.

1. The i.v. administration of tumor necrosis factor-alpha (TNF-alpha), interleukin-8 (IL-8) and the recently described macrophage-derived neutrophil chemotactic factor (MNCF) inhibits the recruitment of neutrophils to the inflammatory site. 2. Pretreatment of mice with the NO synthase antagonist, NG-monomethyl-L-arginine (L-NMMA, 15-60 mg kg(-1)), but not the inactive enantiomer D-NMMA (30 mg kg(-1)), prevented in a dose-dependent manner the TNF-alpha, IL-8 and MNCF-mediated inhibition of neutrophil migration into thioglycollate-challenged peritoneal cavities. 3. Treatment of the neutrophils with TNFalpha (10(-7) M), IL-8 (10(-7) M) or MNCF blocked their migration towards FMLP in the chemotaxis assay. The pretreatment of the neutrophils with L-NMMA (50-200 microM) prevented in a dose-dependent manner the inhibition of FMLP-induced chemotaxis by IL-8, but did not alter the inhibition caused by TNF-alpha or MNCF. Different concentrations of the NO donors, S-nitroso-N-acetylpenicillamine (SNAP) or 3-morpholino-sydnonimine (SIN-1), did not alter this chemotaxis. 4. Preincubating the neutrophils with L-NMMA (200 microM) significantly increased the TNF-alpha (10(-7) M) and MNCF-mediated neutrophil adhesion to unstimulated endothelial cells, but had no effect on IL-8 (10(-7) M)-mediated adhesion. 5. Although NO donors did not directly affect the mechanisms of neutrophil motility, NO is involved in the in vitro inhibitory action of IL-8 on chemotaxis. The TNF-alpha and MNCF-mediated inhibition of neutrophil migration seems to be indirect, by affecting the mechanisms of adhesion. It was concluded that TNF-alpha-, IL-8- and MNCF-mediated inhibition of neutrophil migration is associated with the stimulation of NO production.

Animals↗

PubMed1996

Differential production of nitric oxide by endotoxin-stimulated rat and mouse neutrophils.

There is controversy regarding the evidence for the production of nitric oxide (NO) by neutrophils (PMNs). The present study investigates NO production, as assessed by the biosynthesis of the end products, nitrite and nitrate, in the pellets and supernatants of rat and mouse peripheral blood neutrophils obtained during endotoxemia and of peritoneal carrageenin-elicited PMNs stimulated in vitro with E. coli lipopolysaccharide (LPS). We also investigated the induction of NO synthase by rat and mouse peritoneal cells. The intraperitoneal (ip) administration of LPS to mice (10 mg/kg) and rats (5 mg/kg) significantly increased plasma nitrate concentration by six and 23-fold, respectively. In vivo pretreatment with L-NGmonomethyl arginine (L-NMMA) significantly inhibited this production. Compared to animals injected with PBS, the cell pellets of blood PMNs obtained from mice, but not rats, 2 or 6 h after LPS administration produced significant amounts of nitrite (14 +/- 3 and 18 +/- 2 nmol/mg protein, respectively). Little or no nitrite was found in the incubating medium. In contrast, 6 h after a carrageenin challenge (700 micrograms) peritoneal neutrophils obtained from rats, but not mice, released high concentrations of nitrite into the supernatant during a 24-h period of incubation (34 +/- 0.8 microM). The nitrite concentration of the pellet of these cells was negligible. In contrast to the lack of increase in the amount of nitrite released into the supernatants, the in vitro stimulation of rat PMNs with LPS (10 micrograms/ml) for 24 h did increase intracellular nitrite concentration (from 0.8 +/- 0.07 to 8 +/- 0.3 nmol/mg protein). In mouse PMNs, LPS treatment caused only a small release of nitrite into the incubation medium (14 +/- 1 microM). There was no significant change in nitrite concentration in the cell pellets. These data suggest that rat and mouse neutrophils differ in their ability to produce nitric oxide following stimulation with endotoxin.

Animals↗

PubMed1993

Interference of a neutrophil recruitment inhibitory factor upon the accumulation of inflammatory cells and airway hyperreactivity in sensitized guinea-pigs after intranasal antigen challenge.

1. A neutrophil recruitment inhibitory factor (NRIF) recovered from the crude supernatant of lipopolysaccharide (LPS)-stimulated macrophages inhibited neutrophil migration following both intratracheal and intravenous administration of LPS, but did not alter the pattern of leukopenia/leucocytosis induced by intravenous LPS. 2. The correlation between airway infiltration by inflammatory cells and hyperreactivity in lungs from actively sensitized and challenged guinea-pigs was investigated by use of NRIF. 3. Increased eosinophil counts were found in the bronchoalveolar lavage fluid from guinea-pigs sensitized with 10 micrograms ovalbumin and challenged at day 14 by the intranasal administration of the antigen. The increase was evident 5 h after challenge and persisted at 24 h. Neutrophil numbers were also increased at this time. Pretreatment with NRIF suppressed the leucocyte increase in the bronchoalveolar lavage fluid. 4. Bronchoconstriction and histamine release induced by 3 ng PAF injected into the isolated lungs were increased in challenged guinea-pigs as compared to sensitized but unchallenged controls. Pretreatment of the animals with NRIF did not interfere with this response, but significantly reduced the bronchoconstriction induced by ovalbumin injection. 5. Even though the increased number of inflammatory cells in bronchoalveolar lavage and airway hyperresponsiveness were concomitant, NRIF inhibited cellular infiltration but failed to alter airway hyperreactivity to PAF, demonstrating that these events may occur independently. Conversely, the inhibition of antigen-induced bronchoconstriction by NRIF suggests that this response is dependent upon the emigration of granulocytes.

Administration, Intranasal↗