Navegando por Palavras-chave "chemokines"
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- ItemSomente MetadadadosCervical cerclage placement decreases local levels of proinflammatory cytokines in patients with cervical insufficiency(Mosby-Elsevier, 2017) Monsanto, Stephany P.; Daher, Silvia [UNIFESP]; Ono, Erika [UNIFESP]; Tezotto Pendeloski, Karen Priscilla [UNIFESP]; Traina, Evelyn [UNIFESP]; Mattar, Rosiane [UNIFESP]; Tayade, ChandrakantBACKGROUND: Cervical insufficiency is characterized by premature, progressive dilation and shortening of the cervix during pregnancy. If left unattended, this can lead to the prolapse and rupture of the amniotic membrane, which usually results in midtrimester pregnancy loss or preterm birth. Previous studies have shown that proinflammatory cytokines such as interleukin-1 beta, interleukin-6, interleukin-8, and tumor necrosis factor alpha are up-regulated in normal parturition but are also associated with preterm birth. Studies evaluating such markers in patients with cervical insufficiency have evaluated only their diagnostic potential. Even fewer studies have studied them within the context of cerclage surgery. OBJECTIVES(S): The objective of the study was to evaluate the impact of local and systemic inflammatory markers on the pathogenesis of cervical insufficiency and the effect of cerclage surgery on the local immune microenvironment of women with cervical insufficiency. STUDY DESIGN: We recruited 28 pregnant women (12- 20 weeks' gestation) diagnosed with insufficiency and referred for cerclage surgery and 19 gestational age-matched normal pregnant women as controls. Serum and cervicovaginal fluid samples were collected before and after cerclage surgery and during a routine checkup for normal women and analyzed using a targeted 13-plex proinflammatory cytokine assay. RESULTS: Before surgery, patients with cervical insufficiency had higher levels of interleukin-1b, interleukin-6, interleukin-12, monocyte chemoattractant protein-1 and tumor necrosis factor alpha in cervicovaginal fluid compared to controls, but after surgery, these differences disappeared. No differences were found in serum of insufficiency versus control women. In patients with insufficiency, the levels of interleukin-1b, interleukin-6, interleukin-8, monocyte chemoattractant protein-1, and interferon gamma in cervicovaginal fluid declined significantly after cerclage compared with before intervention, but these changes were not detected in serum. CONCLUSION: Compared with normal women, patients with cervical insufficiency have elevated levels of proinflammatory cytokines in cervicovaginal fluid but not in serum, suggesting a dysregulation of the local immune environment. Cerclage intervention led to a significant decline in these proinflammatory cytokines, suggesting that cerclage may help reduce local inflammation in cervical insufficiency.
- ItemSomente MetadadadosThe chemokines secretion and the oxidative stress are targets of low-level laser therapy in allergic lung inflammation(Wiley-V C H Verlag Gmbh, 2016) Carvalho, Jorge Luis Costa [UNIFESP]; Aparecida de Brito, Aurileia; Ligeiro de Oliveira, Ana Paula; de Castro Faria Neto, Hugo Caire; Pereira, Thiago Martini; Carvalho, Regiane Albertini de [UNIFESP]; Anatriello, Elen [UNIFESP]; Aimbire, Flavio [UNIFESP]Recent studies show that low-level laser therapy (LLLT) has an important anti-inflammatory action in acute lung inflammation. The present work explored if laser therapy is able to antagonize eosinophils and allergic inflammation induced by oxidative stress in Balb/c mice. Forty-eight hours after challenge, the leukocyte counting, ROS and nitrite/nitrate level, RANTES, CCL3, CCL8 as well as eotaxins were measured in the bronchoalveolar lavage fluid (BALF) of laser-treated mice or not. Into the lung, some chemokines receptors, the iNOS activity and mRNA expression, and the activities of superoxide dismutase (SOD), catalase, gluthatione, NADPH oxidase activities and thiobarbituric acid reactive species (T-Bars) were measured. Laser-treated allergic mice presented reduction of both the ICAM-1 and eosinophil in the lungs. RANTES, CCL8, CCL3 and eotaxins were reduced in BALF of laser-treated allergic mice. In allergic mice lung LLLT decreased the CCR1 and CCR3 and restored the oxidative stress balance as well. Laser decreased the lipidic peroxidation in allergic mice lung as much as increased SOD, GPx and GR. It shows that LLLT on allergic lung inflammation involves leukocyte-attractant chemokines and endogenous antioxidant. Based on results, LLLT may ultimately become a non-invasive option in allergic lung disease treatment. [GRAPHICS] The top figure illustrates the laser decreasing the eosinophils migration into BALF and the bottom figure shows the laser upregulating the expression of heme-oxygenase (anti-oxidant enzyme) in lung tissue anti-oxidant.
- ItemSomente MetadadadosComparative analysis of the pathological events involved in immune and non-immune TRALI models(Wiley-Blackwell, 2012-11-01) Tamarozzi, M. B.; Soares, S. G.; Sa-Nunes, A.; Paiva, H. H.; Saggioro, F. P.; Garcia, A. B.; Lucena-Araujo, A. R.; Falcao, R. P.; Bordin, J. O. [UNIFESP]; Rego, E. M.; Universidade de São Paulo (USP); Invent Biotecnol; Universidade Federal de São Paulo (UNIFESP)Background and Objectives Transfusion-related acute lung injury (TRALI) is characterized by leukocyte transmigration and alveolar capillary leakage shortly after transfusion. TRALI pathogenesis has not been fully elucidated. in some cases, the infusion of alloantibodies (immune model), whereas in others the combination of neutrophil priming by proinflammatory molecules with the subsequent infusion of biological response modifiers (BRMs) in the hemocomponent (non-immune model) have been implicated. Our aim was to compare the pathological events involved in TRALI induced by antibodies or BRMs using murine models. Materials and Methods in the immune model, human HNA-2+ neutrophils were incubated in vitro with a monoclonal antibody (anti-CD177, clone 7D8) directed against the HNA-2 antigen and injected i.v. in NOD/SCID mice. in the non-immune model, BALB/c mice were treated with low doses of lipopolysaccharide (LPS) followed by platelet-activating factor (PAF) infusion 2 h later. Forty minutes after PAF administration, or 6 h after neutrophil injection, lungs were isolated and histological analysis, determination of a variety of cytokines and chemokines including keratinocyte-derived chemokine (KC), MIP-2, the interleukins IL-1 beta, IL-6, IL-8 as well as TNFa, cell influx and alveolar capillary leakage were performed. Results in both models, characteristic histological findings of TRALI and an increase in KC and MIP-2 levels were detected. in contrast to the immune model, in the non-immune model, there was a dramatic increase in IL-1 beta and TNFa. However, capillary leakage was only detected if PAF was administrated. Conclusions Regardless of the triggering event(s), KC, MIP-2 and integrins participate in TRALI pathogenesis, whereas PAF is essential for capillary leakage when two events are involved.
- ItemSomente MetadadadosMacrophage signaling by glycosylphosphatidylinositol-anchored mucin-like glycoproteins derived from Trypanosoma cruzi trypomastigotes(Elsevier B.V., 2002-07-01) Ropert, C.; Ferreira, LRP; Campos, MAS; Procopio, D. O.; Travassos, L. R.; Ferguson, MAJ; Reis, LFL; Teixeira, M. M.; Almeida, I. C.; Gazzinelli, R. T.; Fiocruz MS; Universidade Federal de Minas Gerais (UFMG); Ludwig Inst Canc Res; Universidade Federal de São Paulo (UNIFESP); Univ Dundee; Universidade de São Paulo (USP)Activation of cells from the innate immune system has an important role in host resistance to early infection with the intracellular protozoan parasite, Trypanosoma cruzi. Here we review the studies that have identified and structurally characterized the glycosylphosphatidylinositol (GPI) anchors, as parasite molecules responsible for the activation of cells from the macrophage lineage. We also cover the studies that have identified the receptor, signaling pathways as well as the array of genes expressed in macrophages that are activated by these glycoconjugates. We discuss the possible-implications of such response on the host resistance to T. cruzi infection and the pathogenesis of Chagas disease. (C) 2002 Editions scientifiques et medicales Elsevier SAS. All rights reserved.