Navegando por Palavras-chave "IL-10"

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    Analysis of polymorphisms of TNF-alpha, LT-alpha, IL-10, IL-12 and CTLA-4 in patients with warm autoimmune haemolytic anaemia
    (Wiley-Blackwell, 2012-08-01) D'Abronzo, L. S. [UNIFESP]; Barros, M. M. O. [UNIFESP]; Bordin, J. O. [UNIFESP]; Figueiredo, M. S. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Introduction: Autoimmune haemolytic anaemia (AIHA) is defined as the increased destruction of red blood cells (RBCs) in the presence of anti-RBC autoantibodies and/or complement. Its pathogenesis is multifactorial and includes changes in mechanisms of cytokine production and functionality. A number of recent studies have implicated cytokines polymorphisms in the pathogenesis of autoimmune diseases. the aim of this study was to determine the frequency of polymorphisms of tumour necrosis factor alpha (TNF-a), lymphotoxin-a (LT-a), interleukin 10 (IL-10), interleukin 12 (IL-12) and cytotoxic T-lymphocyte antigen-4 (CTLA-4) in patients with AIHA in comparison with healthy individuals. Methods: the study population consisted of 17 patients with AIHA and 40 healthy controls. the polymorphisms for TNF-a-308, LT-a +252, IL-10 -592, IL-12 +1188 and CTLA-4 +49 were examined by polymerase chain reaction followed by specific restriction enzyme digestion. Results: There was no significant difference in the phenotypic distributions of polymorphisms of the TNF-a, IL-10, IL-12 and CTLA-4 between the patients and controls. Compared with healthy controls, patients with AIHA had a significant higher frequency of LT-a (+252) AG phenotype (41%vs. 13%; P = 0.032). Conclusion: in this study, no significant differences on the frequency of TNF-a, IL-10, IL-12 and CTLA-4 polymorphisms between patients with AIHA and controls was found, suggesting that the targeted polymorphisms do not influence on the emergence and evolution of the disease. However, the LT-a +252 polymorphism might have an effect for AIHAI development, suggesting that further studies are necessary to clear up this question.
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    B-1 cell: the precursor of a novel mononuclear phagocyte with immuno-regulatory properties
    (Acad Brasileira De Ciencias, 2009-09-01) Lopes, Jose Daniel [UNIFESP]; Mariano, Mario [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Characterization of the origin, properties, functions and fate of cells is a fundamental task for the understanding of physiological and pathological phenomena. Despite the bulk of knowledge concerning the diverse characteristics of mammalian cells, some of them, such as B-1 cells, are still poorly understood. Here we report the results obtained in our laboratory on these cells in the last 10 years. After showing that B-1 cells could be cultured and amplified in vitro, a series of experiments were performed with these cells. They showed that B1 cells reside mostly in the peritoneal and pleural cavities, migrate to distant inflammatory foci, coalesce to form giant cells and participate in granuloma formation, both in vitro and in vivo. They are also able to present antigens to immunologically responsive cells and are endowed with regulatory properties. Further, we have also shown that these cells facilitate different types of infection as well as tumor growth and spreading. These data are presently reviewed pointing to a pivotal role that these cells may play in innate and acquired immunity.
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    B-1 cells modulate the kinetics of wound-healing process in mice
    (Elsevier B.V., 2010-03-01) Oliveira, H. C. [UNIFESP]; Popi, A. F. [UNIFESP]; Bachi, Andre Luis Lacerda [UNIFESP]; Nonogaki, S.; Lopes, J. D. [UNIFESP]; Mariano, M. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Hosp Canc; Univ Paulista
    Wound healing is a complex phenomenon whose mechanisms are not fully understood. Although inflammatory cells are recruited to the site of the lesion there are no reports concerning the participation of B lymphocytes in tissue repair. As demonstrated in our laboratory, B-1 cells migrate to a non-specific inflammatory focus and differentiate into a phagocyte. It has been reported that BALB/Xid mice are deficient in B-1 cells. Using this model, here we report that BALB/Xid mice have an increased inflammatory response, a delayed wound-healing process, a prominent neutrophilic infiltration of the lesion, and an increased neovascularization of the lesion as compared with BALB/c and BALB/Xid reconstituted with B-1 cells. the infiltration of B-1 cells into the wound was demonstrated. As B-1 cells secret and use interleukin 10 (IL-10) as an autocrine growth factor, the possible participation of this interleukin in the kinetics of wound healing was investigated. Results show that C57/BL6 IL-10 KO mice had an increased inflammatory response when compared with C57/BL6 and C57/BL6 IL-10 KO mice reconstituted with B-1 cells, thus suggesting that the observed effects of B-1 cells in the healing process is mediated by this interleukin. However, the mechanisms by which IL-10 influence these phenomena remain to be uncovered. (C) 2009 Elsevier GmbH. All rights reserved.
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    B16 melanoma cells increase B-1 cell survival, IL-10 production and radioresistance in vitro
    (Elsevier B.V., 2013-04-01) Lucatelli Laurindo, Maria Fernanda [UNIFESP]; Thies, Felipe Garutti [UNIFESP]; Perez, Elizabeth Cristina [UNIFESP]; Novaes e Brito, Ronni Romulo [UNIFESP]; Mariano, Mario [UNIFESP]; Popi, Ana Flavia [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Paulista UNIP
    B-1 cells can be differentiated from B-2 cells because they are predominantly located in the peritoneal and pleural cavities and have distinct phenotypic patterns and activation properties. the role of both cell populations in cancer progression is still controversial. Previous studies have indicated that direct contact between B-1 cells and B16 melanoma tumor cells (B16) increases the metastatic potential of the tumor cells. However, cellular changes that are induced in B-1 cells during the interaction between these two cell types have not been evaluated. in the present study, it is hypothesized that B-1 cells are modified after their interaction with tumor cells, leading to both increased cell viability and rate of proliferation. Additionally, soluble factors that were secreted by B16 cells were sufficient to augment B-1 cell viability and to modify the production of IL-10 by B-1 cells. Impressively, after direct or indirect contact with the B16 cells, B-1 cells became resistant to radiation-induced cell death. Thus, future studies that assess the importance of concomitant immunity and other conventional therapies in cancer treatment are needed. (C) 2012 Elsevier GmbH. All rights reserved.
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    Coacervate whey protein improves inflammatory milieu in mice fed with high-fat diet
    (Biomed Central Ltd, 2014-03-28) Moreno, Mayara Franzoi [UNIFESP]; Souza, Gabriel Inacio de Morais Honorato de [UNIFESP]; Hachul, Ana Claudia Losinskas [UNIFESP]; Santos, Bruno dos [UNIFESP]; Okuda, Marcos Hiromu [UNIFESP]; Pinto Neto, Nelson Inacio [UNIFESP]; Boldarine, Valter Tadeu [UNIFESP]; Esposito, Elisa [UNIFESP]; Ribeiro, Eliane Beraldi [UNIFESP]; Nascimento, Claudia Maria da Penha Oller do [UNIFESP]; Ganen, Aline de Piano [UNIFESP]; Oyama, Lila Missae [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Background: Functional foods with bioactive properties may help in treat obesity, as they can lead to a decreased risks of inflammatory diseases. the aim of this study was to investigate the effects of chitosan coacervate whey protein on the proinflammatory processes in mice fed with high-fat diet.Methods: Mice were divided into two groups receiving either a normolipidic or high-fat diet; the animals in each of the two diet groups were given a diet supplement of either coacervate (gavage, 36 mg protein/kg of body weight) or tap water for four weeks [groups: normolipidic diet plus water (C); normolipidic diet and coacervate (CC); high-fat diet and water (H); and high-fat diet and coacervate (HC)].Results: the high-fat diet promoted inflammation, possibly by decreased adiponectin/sum of adipose tissues ratio and increased phosphorylation of NF-kappa B p50. in HC we observed a positive correlation between IL-10 and TNF-alpha in mesenteric adipose tissue, retroperitoneal adipose tissue and liver tissue. We also observed a positive correlation between lipopolisaccharide with IL-10 in the liver tissue.Conclusions: High-fat diet treatment promoted metabolic alterations and inflammation, and chitosan coacervate whey protein modulated inflammatory milieu.
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    Differential inhibitory mechanism of cyclic AMP on TNF-alpha and IL-12 synthesis by macrophages exposed to microbial stimuli
    (Stockton Press, 1999-07-01) Procópio, Daniela O. [UNIFESP]; Teixeira, Mauro M.; Camargo, Maristela M.; Travassos, Luiz R.; Ferguson, Michael AJ; Almeida, Igor C.; Gazzinelli, Ricardo T.; Universidade Federal de Minas Gerais (UFMG); FIOCRUZ; Universidade Federal de São Paulo (UNIFESP); Univ Dundee
    1 Microbial stimuli such as bacterial lipopolysaccharide (LPS) or glycosylphosphatidylinositol-mucins derived from Trypanosoma cruzi trypomastigotes (tGPI-mucins) are effective stimulators of the synthesis of cytokines by macrophages. Here, we evaluated the ability of cyclic AMP mimetic or elevating agents to modulate TNF-alpha and IL-12 synthesis by murine inflammatory macrophages.2 Cholera Toxin (ChTx) inhibited tGPI-mucins (2.5 nM) or LPS (100 ng ml(-1)) induced TNF-alpha and IL-12(p40) synthesis in a concentration-dependent manner. Similarly, the cyclic AMP mimetics, 8-bromo cyclic AMP or dibutyryl cyclic AMP, or prostaglandin (PG) E-2 inhibited the synthesis of both cytokines by macrophages exposed to microbial stimuli.3 the protein kinase A inhibitor H-89 partially reversed the inhibitory effects of dibutyryl cyclic AMP and PGE(2) on both IL-12(p40) and TNF-alpha synthesis.4 Pretreatment of macrophages with dibutyryl cyclic AMP or ChTx augmented the synthesis of IL-10 triggered by microbial products. Elevation of cyclic AMP inhibited the synthesis of TNF-alpha, but not IL-12(p40), by inflammatory macrophages from IL-10 knockout mice.5 Kinetic studies showed that synthesis of both TNF-alpha and IL-10 peaked at 8 h and IL-12 at 24 h after stimulation with microbial stimuli.6 Together, our findings favour the hypothesis that the cyclic AMP inhibitory activity on IL-12(p40) but not on TNF-alpha synthesis is dependent on de novo protein synthesis, most likely involving IL-10, by macrophages stimulated with microbial products. Accordingly, dibutyryl cyclic AMP inhibited IL-12(p40) synthesis only when added before or at the same time of the stimuli. in contrast, the effect of this cyclic AMP analogue on TNF-alpha synthesis was protracted and observed even 2 h after the addition of the stimuli.
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    Doença de Chagas: aspectos gerais e imunopatogenia com foco para a atuação das células B-1 durante a infecção - uma revisão bibliográfica
    (Universidade Federal de São Paulo, 2022-12-07) Queiroz, Júlia Fonseca [UNIFESP]; Batista, Patricia Xander [UNIFESP]; http://lattes.cnpq.br/3620553457348403
    A doença de Chagas é uma zoonose negligenciada causada pelo protozoário Trypanosoma cruzi, que apresenta grande importância epidemiológica e que nos últimos anos tem se disseminado para fora da área endêmica. Ainda há diversos questionamentos acerca da imunopatogenia da doença de Chagas e a relação parasita-hospedeiro. Estudos realizados demonstram que é muito importante o balanço entre citocinas pró- e anti-inflamatórias para uma resposta imunológica mais efetiva ao parasito, mas não só isso, os efeitos protetivos dependem do background genético do hospedeiro, da virulência da cepa e do inóculo, o que denota grande desafio para o desenvolvimento de novas terapias. Diversos estudos já demonstraram que pacientes na fase crônica exibem anticorpos autorreativos que levam a piora do quadro clínico, mas ainda não se sabe como esses anticorpos são gerados. As células B-1, ainda pouco estudadas, dentre diversas funcionalidades, são capazes de produzir citocinas e anticorpos, incluindo autoanticorpos. Na fase aguda da doença de Chagas os anticorpos aparecem com baixa especificidade e podem perdurar durante longos períodos em mecanismo similar ao que acontece no lúpus eritematoso sistêmico, o que levanta o questionamento sobre a implicação desses anticorpos na evolução da doença. Na fase crônica, uma maior frequência de células B-1 e seu perfil anti-inflamatório parecem ser favoráveis para o hospedeiro. O presente estudo pretende conectar os aspectos gerais da doença de Chagas e a sua imunopatogenia, com foco para a atuação células B-1 durante a infecção, mesmo que poucos estudos tenham sido realizados acerca das implicações dessas células na patologia em questão. Essas células têm papel relevante na doença de Chagas e podem ser protagonistas ou mesmo direcionadoras para o desenvolvimento de novas estratégias terapêuticas no combate a T. cruzi se mais esforços forem realizados para estudá-las no contexto dessa parasitose.
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    Donor bone marrow cells play a role in the prevention of accelerated graft rejection induced by semi-allogeneic spleen cells in transplantation
    (Elsevier B.V., 2008-02-01) Moraes, Luciana V. de; Bueno, Valquiria [UNIFESP]; Marguti, Ivo; Martins, Gislaine A.; Vallochi, Adriana L.; Yamamoto, Guilherme L.; Panajotopoulos, Nicolas; Mengel, Jose O.; Rizzo, Luiz V.; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP); Columbia Univ Coll Phys & Surg; Fundacao Oswaldo Cruz; Fdn Zerbini
    Spleen or spleen plus bone marrow cells from (BALB/c x C57Bl/6)F1 donors were transferred into BALB/c recipients 21 days before skin or cardiac transplantation. Prolonged graft survival was observed on recipients treated with the mixture of donor-derived cells as compared to those treated with spleen cells alone. We evaluated the expression of CD45RB and CD44 by splenic CD4(+) and CD8(+) T cells 7 and 21 days after donor cell transfer. the populations of CD8(+)CD45RB(low) and CD8(+)CD44(high) cells were significantly decreased in mice pre-treated with donor spleen and bone marrow cells as compared to animals treated with spleen cells only, although these cells expanded in both groups when compared to an earlier time-point. No differences were observed regarding CD4+ T cell population when recipients of donor-derived cells were compared. An enhanced production of IL-10 was observed seven days after transplantation in the supernatants of spleen cell cultures of mice treated with spleen and bone marrow cells. Taken together these data suggest that donor-derived bone marrow cells modulate the sensitization of the recipient by semi-allogeneic spleen cells in part by delaying the generation of activated/memory CD8(+) T cells leading to enhanced graft survival. (c) 2007 Elsevier B.V. All rights reserved.
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    Dual Effect of Low-Level Laser Therapy (LLLT) on the Acute Lung Inflammation Induced by Intestinal Ischemia and Reperfusion: Action on Anti- and Pro-Inflammatory Cytokines
    (Wiley-Blackwell, 2011-07-01) Mafra de Lima, Flavia; Villaverde, Antonio Balbin; Albertini, Regiane; Correa, Joao Carlos Ferrari; Carvalho, Rodrigo Leal de Paiva; Munin, Egberto; Araujo, Thiago Rodrigues de; Silva Junior, Jose Antonio; Aimbire, Flavio [UNIFESP]; Univap; Unicastelo; Nove de Julho Univ; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    Background and Objective: It is unknown if pro-and anti-inflammatory mediators in acute lung inflammation induced by intestinal ischemia and reperfusion (i-I/R) can be modulated by low-level laser therapy (LLLT).Study Design/Material and Methods: A controlled ex vivo study was developed in which rats were irradiated (660 nm, 30 mW, 0.08 cm(2) of spot size) on the skin over the right upper bronchus 1 hour post-mesenteric artery occlusion and euthanized 4 hours later. for pretreatment with anti-tumor necrosis factor (TNF) or IL-10 antibodies, the rats received either one of the agents 15 minutes before the beginning of reperfusion.Methods: Lung edema was measured by the Evans blue extravasation and pulmonary neutrophils influx was determined by myeloperoxidase (MPO) activity. Both TNF and IL-10 expression and protein in lung were evaluated by RT-PCR and ELISA, respectively.Results: LLLT reduced the edema (80.1 +/- 41.8 mu g g(-1) dry weight), neutrophils influx (0.83 +/- 0.02 x 10(6) cells ml(-1)), MPO activity (2.91 +/- 0.60), and TNF (153.0 +/- 21.0 pg mg(-1) tissue) in lung when compared with respective control groups. Surprisingly, the LLLT increased the IL-10 (0.65 +/- 0.13) in lung from animals subjected to i-I/R. Moreover, LLLT (0.32 +/- 0.07 pg ml(-1)) reduced the TNF-alpha level in RPAECs when compared with i-I/R group. the presence of anti-TNF or IL-10 antibodies did not alter the LLLT effect on IL-10 (465.1 +/- 21.0 pg mg (1) tissue) or TNF (223.5 +/- 21.0 pg mg (1) tissue) in lung from animals submitted to i-I/R.Conclusion: the results indicate that the LLLT attenuates the i-I/R-induced acute lung inflammation which favor the IL-10 production and reduce TNF generation. Lasers Surg. Med. 43:410-420, 2011. (C) 2011 Wiley-Liss, Inc.
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    Endurance training induces depot-specific changes in IL-10/TNF-alpha ratio in rat adipose tissue
    (Elsevier B.V., 2009-02-01) Lira, F. S.; Rosa, J. C. [UNIFESP]; Yamashita, A. S.; Koyama, C. H.; Batista, M. L.; Seelaender, M.; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP); Univ Mogi das Cruzes
    White adipose tissue (WAT) is the source of pro- and anti-inflammatory cytokines and recently, it has been recognized as an important source of interleukin 10 (IL-10). Acute physical exercise is known to induce an anti-inflammatory cytokine profile, however, the effect of chronic physical exercise on the production of IL-10 by WAT has never been examined. We assessed IL-10 and TNF-alpha concentration in WAT of rats engaged in endurance training. Animals were randomly assigned to either a sedentary control group (S, n = 7) or an endurance trained group (T, n = 8). Trained rats ran on a treadmill 5 days/wk for 8 wk (55-65% VO(2max). Detection of IL-10 and TNF-alpha protein and mRNA expression, as well as the gene expression of PPAR-gamma, and immunocytochemistry to detect mononuclear phagocytes were carried out. A reduction in absolute retroperitoneal adipose tissue (RPAT) weight in T (44%; p < 0.01), when compared with S was observed. IL-10 concentration was increased (1.5-fold, p < 0.05), to a higher extent than that of TNF-alpha (66%. p < 0.05) in the mesenteric adipose tissue (MEAT) of the trained group, while no change related to training was observed in RPAT. in MEAT, IL-10/TNF-alpha ratio was increased in T, when compared with S (30%; p < 0.05). PPAR-gamma gene expression was increased in T (1.1-fold; p < 0.01), when compared with S in the same adipose depot. No monocyte infiltration was found. in conclusion, exercise training induced increased IL-10 expression in the mesenteric depot, resulting in a modified IL-10/TNF-alpha ratio. We also conclude that WAT presents a depot-specific response to endurance training regarding the studied aspects. (C) 2008 Elsevier B.V. All rights reserved.
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    Epstein-Barr viral load, interleukin-6 and interleukin-10 levels in post-transplant lymphoproliferative disease: A nested case-control study in a renal transplant cohort
    (Taylor & Francis Ltd, 2005-04-01) Baiocchi, Otavio Carvalho Guimarães [UNIFESP]; Colleoni, Gisele Wally Braga [UNIFESP]; Caballero, Otávia L.; Vettore, André L.; Bulgarelli, Adriana; Dalboni, Maria Aparecida [UNIFESP]; Granato, Celso Francisco Hernandes [UNIFESP]; Franco, Marcello Fabiano de [UNIFESP]; Pestana, Jose Osmar Medina [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Ludwig Inst Canc Res; Hosp Rim & Hipertensao; Fleury Virol Div
    The possible correlation among Epstein - Barr virus (EBV) load, interleukin-6 (IL-6) and interleukin-10 (IL-10) levels has become an attractive issue and can provide a useful tool for diagnosis and monitoring of patients at risk for post-transplant lymphoproliferative disease (PTLD) development. At the time of diagnosis of PTLD, 11 patients were prospectively enrolled and 55 nested controls were selected from a 1800 renal transplant cohort. Real-time polymerase chain reaction (PCR) was used to quantify EBV load in peripheral blood mononuclear cells (PBMC). Serum IL-6 and IL-10 levels were determined using an enzyme-linked immunosorbent assay ( ELISA). the median EBV load of PTLD cases was 17400 copies/10(6) PBMC, statistically different from controls ( P = 0.001). the median IL-6 level of PTLD cases was not different from controls (P=0.079). However, median IL-10 levels showed a significant difference in both groups ( P <= 0.001). the receiver-operating characteristic (ROC) curve analysis was applied to estimate the IL-10 cut-off value predictive of PTLD development. We found that 73.5 pg/ml has high sensitivity (1.00) and specificity (0.85). Also, Pearson's analysis showed a strong correlation between EBV load and serum IL-10 concentration ( P <= 0.001). This nested case - control study demonstrates that EBV load at diagnosis of PTLD correlates with IL-10 levels, and that monitoring of IL-10 can provide a less expensive and less time-consuming tool for PTLD diagnosis and close follow-up of patients at risk. Furthermore, we were able to de. ne a cut-off value of IL-10 mostly predictive of PTLD development in this cohort. Our data suggest that serial measurements prior to PTLD development must be carried out to validate our hypothesis.
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    Estudo do efeito da manipulação da rede de citocinas sobre o padrão de sono e desempenho de camundongos na tarefa de esquiva inibitória de múltiplas tentativas
    (Universidade Federal de São Paulo (UNIFESP), 2016-03-31) Esumi, Lia Assae [UNIFESP]; Hipólide, Débora Cristina [UNIFESP]; http://lattes.cnpq.br/6303382961871353; http://lattes.cnpq.br/5665138706228728; Universidade Federal de São Paulo (UNIFESP)
    Among the many functions already related to sleep, the relationship of this phenomenon with the memory processing is probably one of the most controversial issues in neuroscience. In attempt to obtain further clarification on this issue, this study aimed to modulate the sleep pattern of mice with the objective of analyze possible changes in memory. To modulate the sleep pattern we used a class of molecules that endogenously participates in sleep regulation ? the cytokines. The anti-inflammatory cytokine interleukin-10 (IL-10) and the pro-inflammatory cytokine IL-12 were administered intraperitoneally into Swiss mice in attempt to modulate the inflammatory profile. There were three purposes: (1) verify the effect of IL-10 and IL-12 treatments in the sleep pattern, (2) verify the effect of IL-10 and IL-12 treatments in the sleep pattern along with the performance in a memory task, and (3) identify possible correlations between sleep pattern and performance on the memory task. To evaluate the sleep pattern, the animals underwent a surgery to implant electrodes for eletrocorticogram and electromyogram recordings. Memory was evaluated through the multiple-trial inhibitory avoidance (MTIA) task. The MTIA task training was performed immediately after treatments, and animals were tested 24h later. Alone, IL-10 and IL-12 treatments did not induce changes in sleep pattern. However, when treatments were conducted immediately before the MTIA task training, the IL-12 group showed decrease in the number of wake, slow-wave sleep (SWS), and paradoxical sleep (PS) episodes; increase in the mean duration of wake episodes; and decrease in the mean duration of PS episodes. Such sleep/wake changes were accompanied by performance improvement of IL-12 group in the EIMT task test. The correlations between the performance on MTIA task and the sleep/wake parameters in the post-training period indicated the contribution of SWS in the first three hours after training, followed by the greater contribuition of the complete cycle, wake? SWS? PS, for the best performance in the EIMT task. We suggest that the superior performance of the IL-12 group is the result of optimization of the memory consolidation process through changes in sleep patterns induced by IL-12 treatment.
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    Interactions between TLR2, TLR4, and mannose receptors with gp43 from Paracoccidioides brasiliensis induce cytokine production by human monocytes
    (Informa Healthcare, 2011-10-01) Nakaira-Takahagi, Erika; Golim, Marjorie A.; Bannwart, Camila F.; Puccia, Rosana [UNIFESP]; Peraçoli, Maria Terezinha Serrão [UNIFESP]; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    The glycoprotein gp43 is an immunodominant antigen secreted by Paracoccidioides brasiliensis, the agent of paracoccidioidomycosis. the present study evaluated whether gp43 can interact with toll-like (TLR2, TLR4) and mannose (MR) receptors on the surface of human monocytes, and how that affects their expression and cytokine production. Monocytes were incubated with or without monoclonal antibodies anti-TLR2, anti-TLR4, or anti-MR, individually or in combination, prior to the addition of gp43. the gp43 binding to monocyte surface, as well as expression of TLR2, TLR4, and MRs were analyzed by flow cytometry, while production of TNF-alpha and IL-10 was monitored by ELISA. the results suggested that gp43 binds to TLR2, TLR4, and MR receptors, with TLR2 and MR having the strongest effect. All three receptors influenced the production of IL-10, while TNF-alpha production was associated with expression of TLR4 and MR. the modulatory effect of gp43 was demonstrated by high levels of TLR4 expression associated with increased production of TNF-alpha after 4 h of culture. Alternatively, high levels of TLR2 expression, and elevated production of IL-10, were detected after 18 h. We showed that interaction between gp43 and monocytes may affect the innate immune response by modulating the expression of the pattern recognition receptors TLR2, TLR4 and MR, as well as production of pro- and anti-inflammatory cytokines.
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    Interleukin-10 secreted by B-1 cells modulates the phagocytic activity of murine macrophages in vitro
    (Blackwell Publishing Ltd, 2004-11-01) Popi, Ana Flavia; Lopes, Jose Daniel [UNIFESP]; Mariano, Mario [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Estadual Paulista
    As demonstrated previously in our laboratory, B-1 cells migrate from the peritoneal cavity of mice and home to a distant site of inflammation to become macrophage-like cells. However, the influence that these cells might have on the kinetics and fate of the inflammatory process is not known. Considering that macrophages are pivotal in the inflammatory reaction, we decided to investigate the possible influence B-1 cells could have on macrophage activities in vitro. Our results show that peritoneal macrophages from Xid mice, a mouse strain deprived of B-1 cells, have higher phagocytic indexes for zymozan particles when compared with macrophages from wild-type mice. Moreover, macrophages from wild-type mice have a lower ability to release nitric oxide and hydrogen peroxide when compared with macrophages from Xid mice. Experiments using cocultures of B-1 cells and macrophages from Xid mice in transwell plates demonstrated that B-1 cells down-regulate macrophage activities. These observations also indicate that this phenomenon is not due to a physical interaction between these two cell populations. As B-1 cells are one of the main sources of interleukin (IL)-10, we demonstrate in this study that adherent peritoneal cells from Xid mice produce significantly less amounts of this cytokine in culture when compared with IL-10 production by cells from wild-type mice. When B-1 cells from IL-10 knock-out mice and macrophages from wild-type mice were cocultured in transwell plates, the phagocytic index of macrophages was not altered demonstrating that B-1 cells can influence the effector functions of macrophages in vitro via IL-10 secretion.
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    Microbicidal property of B1 cell derived mononuclear phagocyte
    (Elsevier B.V., 2009-08-01) Popi, A. F. [UNIFESP]; Zamboni, D. S.; Mortara, R. A. [UNIFESP]; Mariano, M. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP)
    A mononuclear phagocyte derived from B1b cells (B1CDP) has been described. As these cells migrate from the peritoneal cavity to non-specific inflammatory lesion sites and are highly phagocytic via Fc and mannose receptors, their microbicidal ability of these cells was investigated using the Coxiella burnetii cell infection model in vitro. in this report, the pattern of infection and C burnetii phase II survival in B1CDP phagosomes was compared with the pattern of infection of peritoneal macrophages from Xid mice (PM phi) and bone marrow derived macrophages (BMM phi). Infection was assessed by determining the large parasitophorous vacuole formation, the relative focus forming units and the quantification of DAPI (4',6-diamino-2-phenylindole) fluorescence images acquired by confocal microscopy. When compared to macrophages, B1CDP are more permissive to the bacterial infection and less effective to kill them. Further, results suggest that IL-10 secreted by B1 cells are involved in their susceptibility to infection by C burnetti, since B1CDP from IL-10 KO mice are more competent to control C. burnetii infection than cells from wild type mice. These data contribute further to characterize B1CDP as a novel mononuclear phagocyte. (C) 2008 Elsevier GmbH. All rights reserved.
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    Presence of Circulating Levels of Interferon-g, Interleukin-10 and Tumor Necrosis Factor-a in Patients with Visceral Leishmaniasis
    (Instituto de Medicina Tropical, 1998-01-01) Medeiros, Iara Marques De [UNIFESP]; Castelo Filho, Adauto [UNIFESP]; Salomão, Reinaldo [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade Federal do Rio Grande do Norte
    Experimental murine L. major infection is characterized by the expansion of distinct CD4+ T cell subsets. The Th1 response is related to production of IFN-g and resolution of infection, whereas Th-2 response with production of IL-4 and IL-10 and dissemination of infection. The objective of this study was to measure the circulating levels of IFN-g, IL-10 and TNF-a in patients with visceral leishmaniasis (VL) before, during and at the end of therapy and to examine the association between cytokine levels and activity of VL. Fifteen patients with VL were evaluated. The cytokine determinations were done by using the enzyme-linked immunoassay (ELISA) before, during and at the end of therapy. At baseline, we detected circulating levels of IFN-g in 13 of 15 patients (median = 60 pg/ml); IL-10 in 14 of 15 patients (median = 141.4 pg/ml); and TNF-a in 13 of 14 patients (median = 38.9 pg/ml). As patients improved, following antimonial therapy, circulating levels of IL-10 showed an exponential decay (y = 82.34 e 0,10367x, r = 0.659; p < 0.001). IFN-g was no longer detected after 7/14 days of therapy. On the other hand, circulating levels of TNF-a had a less pronounced decay with time on therapy, remaining detectable in most patients during the first seven days of therapy (y = 36.99-0.933x, r = 0.31; p = 0.05). Part of the expression of a successful response to therapy may, therefore, include reduction in secretion of inflammatory as well as suppressive cytokines. Since IL-10 and IFN-g are both detected prior to therapy, the recognized cellular immune depression seen in these patients may be due to biological predominance of IL-10 (type 2 cytokine), rather than lack of IFN-g (type 1 cytokine) production.
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    Production of IFN-gamma is impaired in patients with paracoccidioidomycosis during active disease and is restored after clinical remission
    (B I O S Scientific Publishers Ltd, 2000-06-01) Karhawi, Abdon Salam Khaled [UNIFESP]; Colombo, Arnaldo Lopes [UNIFESP]; Salomão, Reinaldo [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Cellular immunity is usually suppressed during paracoccidioidomycosis (PCM) and is restored after treatment. in this study we evaluated the induction of a type 1 (interferon gamma (IFN-gamma)), a type 2 (interleukin (IL)-10) and a primarily macrophage derived cytokine (tumor necrosis factor (TNF)-alpha) in peripheral blood mononuclear cells (PBMC) from patients with PCM. Eight male patients with active PCM, nine male patients with clinical remission of the disease and 10 healthy control subjects were enrolled in the study. Cytokines were induced with non-specific stimuli - phytohaemagglutin (PHA) (induces IL-10 and IFN-gamma), Lipopolysaccharide (induces TNF-alpha) - and Paracoccidioides brasiliensis antigen (PbAg) (induces IL-10, IFN-gamma and TNF-alpha). Induction of IFN-gamma with PHA differed among the three groups (P < 0.01; Kruskal-Wallis test) and with PbAg was lower in patients with active disease compared to those in clinical remission (P = 0.05; Mann-Whitney). Induction of IL-10 and of TNF-alpha was similar in the three groups. the suppressed production of IFN-gamma in patients with active disease may underscore the cellular immune deficiency seen in these patients.
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    TLR2, TLR4, CD14, CD11b, and CD11c expressions on monocytes surface and cytokine production in patients with sepsis, severe sepsis, and septic shock
    (Lippincott Williams & Wilkins, 2006-04-01) Brunialti, Milena Karina Coló [UNIFESP]; Martins, Paulo Sergio [UNIFESP]; Carvalho, Heraclito Barbosa DE [UNIFESP]; Machado, Flávia Ribeiro [UNIFESP; Barbosa, L. M.; Salomão, Reinaldo [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP); Santa Marcelina Hosp
    Bacterial recognition and induced cellular activation are fundamental for the host control of infection, yet the limit between protective and harmful response is still inexact. Forty-one patients were enrolled in this study: 14 with sepsis, 12 with severe sepsis, and 15 with septic shock. Seventeen healthy volunteers (HV) were included as control. the expression of TLR2, TLR4, CD14, CD11b, and CD11c was analyzed on monocytes surface in whole blood. sCD14 was measured in serum, and TNF-alpha, IL-6, and IL-10 cytokine levels were measured in PBMC supernatants after LIPS, IL-1 beta, and TNF-alpha stimuli by ELISA. An increase in sCD14 and a decreased mCD14 were found in patients as compared with HV (P < 0.001). However, no differences in the expression of TLR2, TLR4, and CD11c were found among the groups. A trend toward differential expression of CD11b was observed, with higher values found in patients with sepsis as compared with HV. A negative regulation of the inflammatory cytokine production was observed in patients with severe sepsis and shock septic in relation to sepsis and HV, regardless of the stimulus. No significant difference in IL-10 production was found among the groups. in this study, we show that the inflammatory response is associated with the continuum of clinical manifestations of sepsis, with a strong inflammatory response in the early phase (sepsis) and a refractory picture in the late phases (severe sepsis and septic shock). Correlation between cell surface receptors and cytokine production after IL-1 beta and TNF-alpha stimuli and the observation of a single and same standard response with the different stimulus suggest a pattern of immunology response that is not dependent only on the expression of the evaluated receptors and that is likely to have a regulation in the intracellular signaling pathways.