Navegando por Palavras-chave "endotoxin"
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- ItemSomente MetadadadosAcute renal failure and the sepsis syndrome(Blackwell Publishing Inc, 2002-02-01) Schor, Nestor; Madias, N. E.; Malnic, G.; Cendoroglo Neto, Miguel [UNIFESP]; Yu, L.; Santos, ODR; Burdmann, E.; Machado, D.; Batista, P. B.; Universidade Federal de São Paulo (UNIFESP); Tufts Univ; Universidade de São Paulo (USP); Universidade Federal do Rio de Janeiro (UFRJ); Sao Jose Do Roi Preto Med Sch; Escola Baiana Med & Saude Publ
- ItemSomente MetadadadosAlterations of heparan sulfate moieties in cultured endothelial cells exposed to endotoxin(Academic Press Inc Jnl-comp Subscriptions, 1996-01-01) Colburn, P.; Dietrich, C. P.; Buonassisi, V; Universidade Federal de São Paulo (UNIFESP)In previous studies, we observed that exposure to endotoxin markedly reduces the level of heparan sulfate proteoglycans in the extracellular matrix of cultured endothelial cells and at the same time causes the accumulation of proteoglycans bearing glycosaminoglycan chains of reduced size in the conditioned medium (P. Colburn, E. Kobayashi, and V. Buonassisi, 1994, J. Cell. Physiol. 159, 121-130). We have now investigated the structural and ligand-binding features which distinguish the matrix glycosaminoglycan moiety and the nature of the alterations of the truncated glycosaminoglycans. the matrix glycosaminoglycans are less sulfated than those of other cellular compartments and are more extensively degraded by heparitinase I, yielding a larger proportion of smaller oligosaccharides. in the binding assays, matrix glycosaminoglycans had greater specificity than those of the cell surface for a synthetic peptide patterned on the carboxyl-terminal sequence of an N-glycan sulfated protein synthesized by the endothelial cell. the nature of the alteration caused by exposure to endotoxin consists in the loss of a region rich in sulfate, located at the nonreducing end of the glycosaminoglycan chain, We also determined that only proteoglycans with intact chains are found in the extracellular matrix of endotoxin-treated cells. (C) 1996 Academic Press, Inc.
- ItemSomente MetadadadosCD163 and CD206 expression does not correlate with tolerance and cytokine production in LPS-tolerant human monocytes(Wiley, 2017) Alves-Januzzi, Amanda Barba [UNIFESP]; Colo Brunialti, Milena Karina [UNIFESP]; Salomao, Reinaldo [UNIFESP]BackgroundLipopolysaccharide (LPS)-tolerant monocytes produce small amounts of inflammatory cytokines, which is one of the characteristics of the alternative activated macrophages (AAM). These cells exhibited an increased expression of CD206 and CD163. Given the functional similarities of AAMs with the modulation of monocytes' functions observed during sepsis and LPS-tolerance, we evaluated whether the inhibition of inflammatory cytokine production by LPS-tolerant monocytes is associated with the phenotype of cells expressing CD206 and CD163. MethodsWe investigated whether tolerant human monocytes would modulate their expression of CD206 and CD163, markers of alternative activation, and whether the level of their expression would be related to cytokines detection. Tolerance to LPS was induced in peripheral blood mononuclear cell by pre-incubating the cells with increasing concentrations of LPS. The expression of CD206 and CD163 and intracellular TNF- and IL-6 was determined 24 h after LPS challenge by flow cytometry. ResultsNo differences in CD163 expression were observed between tolerant and non-tolerant cells, while the expression of CD206, which was decreased following LPS stimulation in non-tolerized cells, was further reduced in tolerant cells. Decreased production of inflammatory cytokines was observed in the tolerized cells, regardless of the expression of CD163 and CD206, with the exception of IL-6 in CD206+ monocytes, which was similarly expressed in both tolerized and non-tolerized cells. ConclusionsThe effect of LPS in the expression of CD163 and CD206 on monocytes is not reverted in LPS tolerant cells, and the inhibition of inflammatory cytokines in tolerant cells is not related with modulation of these receptors. (c) 2016 International Clinical Cytometry Society
- ItemSomente MetadadadosDaycare centers and schools as sources of exposure to mites, cockroach, and endotoxin in the city of São Paulo, Brazil(Mosby, Inc, 2002-10-01) Rullo, Vera Esteves Vagnozzi [UNIFESP]; Rizzo, Maria Candida Faria Varanda [UNIFESP]; Arruda, L. K.; Solé, Dirceu [UNIFESP]; Naspitz, Charles Kirov [UNIFESP]; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)Background: Public places, including schools, have been identified as sources of exposure to allergens derived from mites, cockroach, cat, and dog and to endotoxin.Objectives: the purposes of this study were to assess and compare exposure to allergens and endotoxin in 4 types of public child-care facilities in Brazil and to investigate whether the presence of children and the performance of cleaning procedures could have an influence on allergen and endotoxin levels. Methods: We have analyzed dust from bedding, floors, chairs, and tables of daycare centers (DCs), preschools, kindergartens, and elementary schools (ESs). Major allergens from mites, cockroach, cat, and dog were quantitated by means of ELISA, and endotoxin content was determined by using the Limulus Amebocyte Lysate assay.Results: Group 1 mite allergens were greater than 2 mug/g in 67% of DC and preschool samples and in 8.9% and 2.2% of kindergarten and ES samples, respectively. the presence of bedding in DCs and preschools accounted for increased levels of mite allergens in these settings. Levels of Bla g I were higher in ES floors compared with those found in DC and preschool floors. Low levels (<1 mug/g) of Fel d 1 e Can f 1 were found in most samples. Levels of endotoxin in DCs and preschools were 3 times higher than in ESs.Conclusions: DCs and schools in Brazil should be considered as important sources of exposure to dust mites and cockroach allergens and to endotoxin. Recommendations for mite allergen avoidance should include appropriate care of bedding in DCs and preschools.
- ItemSomente MetadadadosDifferent mechanism of LPS-induced vasodilation in resistance and conductance arteries from SHR and normotensive rats(Nature Publishing Group, 2002-09-01) Farias, Nelson C.; Borelli-Montigny, Gisele L.; Fauaz, Grasiele; Feres, Teresa; Borges, Antonio Carlos R [UNIFESP]; Paiva, Therezinha B. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)1 the direct and endothelium-dependent effects of lipopolysaccharide (LPS) were investigated on resistance and conductance arteries from normotensive Wistar (NWR) and spontaneously hypertensive (SHR) rats.2 in both NWR and SHR, LPS induced dose-dependent relaxations of the mesenteric vascular bed, which were inhibited by L-NNA in SHR but not in NWR. Iberiotoxin (IBTX) inhibited the responses to LPS in both groups, indicating the participation of high conductance Ca2+-dependent K+ channels.3 in mesenteric artery rings, the resting membrane potentials and the hyperpolarizing responses of NWR to LPS did not differ in endothelized and denuded preparations but L-NNA inhibited the responses only in endothelized rings. These responses were reduced by bosentan, suggesting that endothelin release may mask a possible hyperpolarizing response to LPS. the hyperpolarizing responses to LPS were blocked by IBTX in both endothelized and de-endothelized NWR rings. in the SHR only intact rings showed hyperpolarization to LPS, which was inhibited by IBTX and by L-NNA.4 in SHR aortic endothelized or denuded rings, LPS induced hyperpolarizing responses which, in endothelized rings, were partially blocked by L-NNA, by IBTX or by glibenclamide, but totally abolished by IBTX plus glibenclamide. No response to LPS was observed in NWR aortic rings.5 Our results indicate that LPS activates large conductance Ca2+-sensitive K+ channels located in the smooth muscle cell membrane both directly and indirectly, through NO release from the endothelium in NWR, whereas NO is the major mediator of the LPS responses in SHR resistance vessels.
- ItemSomente MetadadadosEscherichia coli lipopolysaccharide impairs the calcium signaling pathway in mesangial cells: role of angiotensin II receptors(Soc Experimental Biology Medicine, 2010-06-01) Maquigussa, Edgar [UNIFESP]; Arnoni, Carine P. [UNIFESP]; Cristovam, Priscila C. [UNIFESP]; Oliveira, Andrea S. de [UNIFESP]; Higa, Elisa M. S. [UNIFESP]; Boim, Mirian A. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Sepsis causes impaired vascular reactivity, hypotension and acute renal failure. the ability of the Escherichia coli endotoxin (lipopolysaccharide [LPS]) to impair agonist-induced contractility in mesangial cells, which contributes to LPS-induced renal dysfunction, was evaluated. Agonist-induced intracellular calcium ([Ca(2+)]i) mobilization was analyzed using angiotensin II (AngII). the effect of LPS on the levels of the renin-angiotensin system (RAS) components and the roles of vasodilatation-inducing molecules including AT2 receptor (AT2R) and nitric oxide (NO) in the cell reactivity were also evaluated. Confluent human mesangial cells (HMCs) were stimulated with LPS (0111-B4, 100 mu g/mL). AngII-induced [Ca(2+)]i mobilization was measured by fluorometric analysis using Fura-2AM in the absence and presence of an AT2R antagonist (PD123319). the mRNA and protein levels for angiotensinogen, renin, angiotensin-converting enzyme, AT1R and AT2R were analyzed by realtime reverse transcriptase-polymerase chain reaction and Western blot, respectively. NO production was measured by the chemiluminescence method in the culture media after 24, 48 and 72 h of LPS incubation. After 24 h, LPS-stimulated HMCs displayed lower basal [Ca(2+)]i and an impaired response to AngII-induced rise in [Ca(2+)]i. LPS significantly increased AT2R levels, but did not cause significant alterations of RAS components. PD123319 restored both basal and AngII-induced [Ca(2+)]i peak, suggesting an involvement of AT2R in these responses. the expected increase in NO production was significant only after 72 h of LPS incubation and it was unaffected by PD123319. Results showed that LPS reduced the reactivity of HMCs to AngII and suggest that the vasodilatation induced by AT2R is a potential mediator of this response through a pathway independent of NO.
- ItemSomente MetadadadosIL-12 inhibits endotoxin-induced inflammation in the eye(Vch Publishers Inc, 1996-05-01) Whitcup, S. M.; Rizzo, L. V.; Lai, J. C.; Hayashi, S.; Gazzinelli, R.; Chan, C. C.; NIH; Universidade Federal de São Paulo (UNIFESP); NIAID; Universidade Federal de Minas Gerais (UFMG)Interleukin-12 (IL-12) is a heterodimeric cytokine that induces interferon (IFN)-gamma production and an increased generation of Th 1 cells. Both IL-12 and IL-12 antagonists are being studied for the treatment of allergic reactions, autoimmune disease and malignancy. the goal of the present experiments was to examine the importance of IL-12 in endotoxin-induced ocular inflammation. the number of inflammatory cells infiltrating eyes with endotoxin-induced uveitis (EIU) was significantly increased in animals treated with intraperitoneal anti-IL-12 antibody when compared to control animals, but there was no difference in infiltrating inflammatory cells in the eyes of animals treated with IL-12 when compared to controls. in contrast, intraocular injection of IL-12 significantly inhibited the development of endotoxin-induced intraocular inflammation. the inflammatory cells were reduced in the eves of animals receiving intraocular IL-obtained from eyes with EIU showed increased levels of IFN-gamma and decreased levels of IL-6 in eyes receiving intraocular IL-12. These data show that IL-12 has an inhibitory effect on endotoxin-induced inflammation in the eye and su that IL-12 can have an immunoregulatory function in some forms of inflammatory disease.
- ItemSomente MetadadadosLeukocytes from wheezing infants release lower amounts of IL-12 and IFN-gamma compared to non-wheezing infants(Wiley-Blackwell, 2012-10-01) Falcai, Angela; Soeiro Pereira, Paulo Vitor; Kubo, Christina Arslanian; Rullo, Vera; Errante, Paolo Rugero; Sole, Dirceu [UNIFESP]; Condino-Neto, Antonio; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP); Santos Med SchObjective This study investigated environmental endotoxin exposure during early life, sensitization to aeroallergens, the production of cytokines by LPS-stimulated leukocytes, and the development of a wheezing phenotype in a prospective cohort of infants with high risk of developing allergic diseases. Materials and Methods Eighty-four infants were followed from birth until 30 months of age. We assessed endotoxin concentration in house dust of their homes during the first 6 months of life. At age 30 months they were clinically evaluated to determine the development of wheezing and other clinical events, were skin prick tested, and had blood samples collected for the evaluation of cytokine release by LPS-stimulated peripheral blood mononuclear cells (PBMC). Results the level of endotoxin exposure during early life was not associated with development of a wheezing phenotype. On the other hand a higher incidence of respiratory infections occurred among recurrent wheezing (RW) infants. PBMC from RW children exposed to higher levels of environmental endotoxin (above 50?EU/mg) released less Interleukin (IL)-12p70 and IFN-? compared to the non-RW group. TNF-a, IL-10, IL-4, IL-5, and IL17 production by LPS-stimulated PBMC from RW and non-RW children was equivalent in both groups of environmental endotoxin exposure. Conclusion in this prospective cohort of infants with high risk of developing allergic diseases we observed that RW and non-RW children were exposed to similar levels of endotoxin early in life. LPS-stimulated PBMC from RW infants exposed to higher levels of endotoxin released significantly less IL-12 and IFN-? compared to non-RW infants. Pediatr Pulmonol. 2012. 47:10541060. (C) 2012 Wiley Periodicals, Inc.
- ItemSomente MetadadadosNasal provocation test (NPT) with isolated and associated Dermatophagoides pteronyssinus (Dp) and Endotoxin lipopolysaccharide (LPS) in children with allergic rhinitis (AR) and nonallergic controls(Hogrefe & Huber Publishers, 2004-01-01) Braga, C. R.; Rizzo, MCV; Naspitz, C. K.; Sole, D.; Universidade Federal de São Paulo (UNIFESP)Background: Inhalation of endotoxin may enhance inflammatory airway response in sensitized asthmatics persons after allergen(s) inhalation.Objective: To evaluate nasal response to intranasal instillation of Dermatophagoides pteronyssinus (Dp), endotoxin (LPS), and to Dp+LPS in children with perennial allergic rhinitis (PAR).Methods: 10 PAR children (positive skin prick test to Dp) and 10 nonallergic controls (C) undergoing nasal provocation test (NPT), who were quantified by active anterior rhinomanometry and measurement of Total Nasal Resistance (TNR). The NPTs were initially performed with histamine (H; 0.03 to 16.0 mg/mL), and then, at least at weekly intervals, the NPTs were done with Dp (1/100,000 to 1/2.5), LPS (1 to 500 mg/mL) and to Dp+LPS. During NPT with Dp+LPS, Dp concentration was kept constant (1/100,000; 1/10,000; 1/1,000) and was combined with different concentrations of LPS (1, 5, 10 20 mg/mL). The NPT was considered positive when TNR reached twice the basal TNR.Results: H and Dp NPTs were positive in all AR children. In group C, H NPT was positive in 60% and Dp NPT was negative in all children. NPT with LPS was positive only in 30% of the AR children. NPT with Dp+LPS was positive in 90% of the AR patients in Dp concentration of 1/1,000 and in LPS concentrations of 5, 10, and 20 mcg/ mL. This positive association was observed with Dp concentrations lower than those obtained during NPT with Dp in 60% of AR patients. There were no changes in pulmonary function tests in all children after NPT.Conclusions: This study suggests that LPS enhances the effects of allergen challenges on nasal airflow. The daily inhalation of allergens plus endotoxin in AR patients does increase the nasal responsiveness.