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Item Are the polymorphisms in ACE and ESR1 genes associated with preeclampsia occurrence?(2019) Lopes, Ana Cristina dos Santos; Perucci, Luiza Oliveira; Evangelista, Fernanda Cristina Gontijo; Godoi, Lara Carvalho; Sabino, Adriano de Paula; Silva, André Talvani Pedrosa da; Dusse, Luci Maria Sant'Ana; Alpoim, Patrícia NessrallaItem Association among ACE, ESR1 polymorphisms and preeclampsia in Brazilian pregnant women.(2019) Lopes, Ana Cristina dos Santos; Perucci, Luiza Oliveira; Evangelista, Fernanda Cristina Gontijo; Godoi, Lara Carvalho; Sabino, Adriano de Paula; Gomes, Karina Braga; Silva, André Talvani Pedrosa da; Dusse, Luci Maria Sant'Ana; Alpoim, Patrícia NessrallaBackground: Genetic, immune and environmental factors are involved in preeclampsia (PE) etiopathogenesis. Considering that hypertension and poor placental perfusion are important features in PE, polymorphisms in the angiotensin-converting enzyme (ACE) and estrogen nuclear receptor 1 (ESR1) genes could be involved in the predisposition and/or development of the disease. The aim of this study was to evaluate if polymorphisms in ACE and ESR1 genes were associated with PE occurrence. Material and Methods: This case-control study included 209 Brazilian pregnant women (107 with severe PE and 102 normotensive controls). The polymorphisms were investigated by polymerase chain reaction (PCR) followed by polyacrylamide gel electrophoresis. Results: No significant difference between PE versus normotensive pregnant women, as well as early versus late PE, was observed when compared the allelic and genotypic frequencies of insertion/deletion polymorphism in intron 16 of the ACE gene and the single nucleotide polymorphisms (SNPs - rs2234693 and rs9340799) of the ESR1 gene. Conclusion: This pioneer study involving Brazilian women showed no association among the studied polymorphisms and PE, which suggests that ins/del ACE and SNPs ESR1 do not contribute to this disease occurrence in Brazil.Item Effects of the phototherapy (blue light) on the heart inflammatory response induced by Trypanosoma cruzi in mice.(2019) Ivanova, Natalia; Silva, André Talvani Pedrosa da; Bianchi, Rodrigo Fernando; Silva, André Talvani Pedrosa da; Silva, Maria Cláudia da; Perucci, Luiza Oliveira; Rezende, Simone AparecidaThe Trypanosoma cruz, is the causative agent of Chagas disease. According to WHO (2019), currently about 7 million people are infected with T. cruzi mainly in Latin America. Despite the fact that pharmaceutical industry releases various new drugs every year, Chagas disease has only two standard substances for treatment, Benznidazole and Nifurtimox, which were recognized as chemotherapy. However, at the same time these medicines have many side effects and are inefficient in chronic phase. Nowadays the blue light is commonly used in medicine practice around the world. It was proved its antimicrobial characteristics. In the current study, were evaluated the influence of the blue light on the inflammatory parameters in C57BL6 mice (in vivo) infected with T. cruzi and as well as development of parasites in vitro. For in vitro experiment we used Y and CL strain of T. cruzi. The blue light was applied (with the pic 460 nm and 80 μW/cm2) on parasite cell culture for 5 days, 6h per day, at room temperature. The parasites were counted in 10 μL every day using the Neubauer Chamber. Treatment with the blue light led to the reduction of replication of T. cruzi in vitro. Data showed 50% reduction of parasites in experiment after 5 days of exposition, in comparison to control. For in vivo experiment was used Y strain of T. cruzi. 40 animals were separated into 4 groups: non-infected + conventional light, non-infected + blue light, infected + conventional light, and infected + blue light. Blue light was applied (with the pic 460 nm and 7 μW/cm2) for 9 days, 12 h per day. Was found that phototherapy with blue light reduce quantity of parasites circulating in the blood of animals comparing with conventional light. Blue light altered the plasma pattern of the inflammatory and regulatory mediators. After morphological analysis, was found that both infected groups exhibited parasitized cardiomyocytes with intense myocarditis with predominance of pericellular and perivascular mononuclear inflammatory infiltrate. Phototherapy with blue light reduced the quantity amastigote in the nests in cardiac tissue. These data can be used for the development of a new way of treatment for Chagas disease in the future.Item Hepatoprotective, antioxidant, anti-inflammatory, and antiviral activities of silymarin against mayaro virus infection.(2021) Ferraz, Ariane Coelho; Almeida, Letícia Trindade; Caetano, Camila Carla da Silva; Menegatto, Marília Bueno da Silva; Lima, Rafaela Lameira Souza; Senna, João Pinto Nelson de; Cardoso, Jamille Mirelle de Oliveira; Perucci, Luiza Oliveira; Silva, André Talvani Pedrosa da; Lima, Wanderson Geraldo de; Silva, Breno de Mello; Reis, Alexandre Barbosa; Magalhães, José Carlos de; Magalhães, Cíntia Lopes de BritoInfection caused by Mayaro virus (MAYV) is responsible for causing acute nonspecific fever, in which the ma- jority of patients develop incapacitating and persistent arthritis/arthralgia. Mayaro fever is a neglected and underreported disease without treatment or vaccine, which has gained attention in recent years after the competence of Aedes aegypti to transmit MAYV was observed in the laboratory, coupled with the fact that cases are being increasingly reported outside of endemic forest areas, calling attention to the potential of an urban cycle arising in the near future. Thus, to mitigate the lack of information about the pathological aspects of MAYV, we previously described the involvement of oxidative stress in MAYV infection in cultured cells and in a non- lethal mouse model. Additionally, we showed that silymarin, a natural compound, attenuated MAYV-induced oxidative stress and inhibited MAYV replication in cells. The antioxidant and anti-MAYV effects prompted us to determine whether silymarin could also reduce oxidative stress and MAYV replication after infection in an immunocompetent animal model. We show that infected mice exhibited reduced weight gain, hepatomegaly, splenomegaly, anaemia, thrombocytopenia, leukopenia, increased liver transaminases, increased pro- inflammatory cytokines and liver inflammation, increased oxidative damage biomarkers, and reduced antioxi- dant enzyme activity. However, in animals infected and treated with silymarin, all these parameters were reversed or significantly improved, and the detection of viral load in the liver, spleen, brain, thigh muscle, and footpad was significantly reduced. This work reinforces the potent hepatoprotective, antioxidant, anti- inflammatory, and antiviral effects of silymarin against MAYV infection, demonstrating its potential against Mayaro fever disease.Item High-sugar diet intake, physical activity, and gut microbiota crosstalk : implications for obesity in rats.(2020) Neves, Viviano Gomes de Oliveira; Oliveira, Daiane Teixeira de; Oliveira, Deborah Campos; Perucci, Luiza Oliveira; Santos, Talita Adriana Pereira dos; Fernandes, Isabela da Costa; Sousa, Graziele Galdino de; Barboza, Natália Rocha; Cota, Renata Guerra de SáThis study aims to evaluate the effect of long-term high-sugar diet (HSD) intake and regular physical activity on gut microbiota as well as its health impact. Weaned male Wistar rats were fed with standard chow diet (SSD) or HSD ad libitum and subjected or not to regular swimming training with a workload (2% of body weight) for 15 weeks. Feces samples were used on microbiome analysis using 16S rRNA amplicon sequencing. HSD increased body mass, adipose cushions, and the serum levels of triglycerides and VLDL, also changed the bacteria taxons associated with metabolic disorders (increase taxons belonging to Proteobacteria phylum and decrease Pediococcus genus); the swim training reverted these changes. SSD intake increased the abundance of bacteria associated with metabolization of dietary fiber. Training in association with SSD consumption beneficially modulated the microbiota, increasing the Bacteroidetes, Bacteroidaceae, Porphyromonadaceae, Parabacteroides, and Lactobacillaceae, and decreasing the Firmicute/Bacteroidetes ratio; training was not able to maintain this profile in animals SHD-fed. Physical training modulates the gut microbiota reversing the obesogenic response caused by SHD. However, training itself is not efficient for up-regulating the probiotic bacteria in comparison to its association with a balanced diet.Item Insights into IL-33 on inflammatory response during in vitro infection by Trypanosoma cruzi.(2022) Oliveira, Daniela Silva de; Leite, Ana Luísa Junqueira; Pedrosa, Tamiles Caroline Fernandes; Mota, Ludmilla Walter Reis; Costa, Guilherme de Paula; Souza, Débora Maria Soares de; Perucci, Luiza Oliveira; Silva, André Talvani Pedrosa daInflammatory and regulatory cytokines play an important role in the immunopathogenesis of Trypanosoma cruzi infection. Interleukin (IL)-33 is a member of the IL-1 superfamily of cytokines whose expression/production is upregulated following pro-inflammatory stimulation to alert the immune system in response to tissue stress or damage. The aim of this study was to evaluate the inflammatory profile induced in cultured J774 cells stimulated or not with IL-33 (10 ng/mL), with live parasites (1 × 106 metacyclic trypomastigote forms) and/or total antigen, TcAg (100 μg/mL) and with both, IL-33 and TcAg/T. cruzi. The cultures were evaluated at 24 h and 48 h after addition of the stimuli. For this, the supernatants were collected for the measurement of TNF, IL-17, CCL2, and IL-10 by ELISA and of nitrite by the Griess method. TNF, IL-17, and CCL2 concentrations were elevated in the presence of TcAg or live T. cruzi parasites at 24 h, and the addition of IL-33 potentiated these effects at 48 h. In addition, the T. cruzi-amastigote forms reduced in those infected J774 cells stimulated with IL-33 at 48 h. In conclusion, the IL-33 elevated the production of the TNF, IL-17, and CCL2 in cultured J774 cells stimulated with T. cruzi and/or its antigen and reduced the intracellular parasites, providing impetus to new investigations on its potential actions on the parasite-induced inflammation.Item Longitudinal assessment of D-dimer and plasminogen activator inhibitor type-1 plasma levels in pregnant women with risk factors for preeclampsia.(2019) Lucena, Flávia Campos; Lage, Eura Martins; Teixeira, Patrícia Gonçalves; Barbosa, Alexandre Simões; Diniz, Rejane Silva; Lwaleed, Bashir; Silva, André Talvani Pedrosa da; Alpoim, Patrícia Nessralla; Perucci, Luiza Oliveira; Dusse, Luci Maria Sant'AnaObjective: Investigating D-Dimer/D-Di and plasminogen activator inhibitor type-1/PAI-1 levels throughout gestation in women with preeclampsia/PE risk factors. Methods: D-Di and PAI-1 plasma levels were determined in 28 women at 12–19, 20–29, 30–34 and 35–40 weeks of gestation. Results: D-Di was lower at 12–19 weeks and higher at 30–34 weeks in women who developed PE versus who did not develop it. D-Di increased throughout gestation in both groups, peaking earlier in pregnant women who developed PE versus who did not develop it. PA1-1 increased across gestation, but it didn’t differ between groups. Conclusion: D-Di was able to discriminate these groups of women at 12–19 and 30–34 weeks of gestation.Item Neuroserpin : a potential biomarker for early-onset severe preeclampsia.(2023) Perucci, Luiza Oliveira; Silva, Sirlaine Pio Gomes da; Bearzoti, Eduardo; Pinto, Kelerson Mauro de Castro; Alpoim, Patrícia Nessralla; Pinheiro, Melina Barros; Godoi, Lara Carvalho; Moraes, Lauro Ângelo Gonçalves de; Sousa, Lirlândia Pires de; Dusse, Luci Maria Sant'Ana; Silva, André Talvani Pedrosa daPreeclampsia is a hypertensive disease of pregnancy associated with intense inflammatory and pro-coagulant responses. Neuroserpin is a serine protease inhibitor that has been involved in neurological and immune pro- cesses and has not yet been investigated in preeclampsia. Herein, we evaluated neuroserpin levels in association with other inflammatory mediators (IL-17A, IL-33, and CXCL-16) during severe preeclampsia. The mediators’ plasma levels were measured by immunoassays in 24 pregnant women with severe preeclampsia (early pre- eclampsia: N = 17, late preeclampsia: N = 7), 34 normotensive pregnant women, and 32 non-pregnant women. In general, pregnancy was associated with higher levels of neuroserpin, IL-17A, IL-33, and CXCL-16 than the non- pregnant state. However, this increase was attenuated in pregnancies complicated by severe preeclampsia. Although neuroserpin levels did not differ between normotensive pregnant women and pregnant women with severe preeclampsia, neuroserpin levels tended to be lower in early-onset than in late-onset severe preeclampsia. There were positive correlations between neuroserpin and IL-17A, neuroserpin and CXCL-16, and IL-17A and CXCL-16 levels in women with severe preeclampsia. In addition, although the risk for developing severe pre- eclampsia was higher in older women in this study, maternal age did not significantly influence the mediators’ levels, nor their correlations in the preeclampsia group. In summary, our data suggest that neuroserpin might be a potential biomarker for early-onset severe preeclampsia and, that the imbalance among neuroserpin, IL-17A, IL-33, and CXCL-16 levels may be associated with the pathogenesis of preeclampsia, regardless of the maternal age.Item Perfil de mediadores inflamatórios produzido por células da linhagem J774 após estímulo in vitro com a IL-33 e antígeno/parasito o Trypanosoma cruzi.(2020) Oliveira, Daniela Silva de; Silva, André Talvani Pedrosa da; Perucci, Luiza Oliveira; Silva, André Talvani Pedrosa da; Perucci, Luiza Oliveira; Estanislau, Juliana de Assis Silva Gomes; Isoldi, Mauro CésarNa infecção pelo protozoário Trypanosoma cruzi, citocinas de perfil inflamatório exercem importante papel na imunopatogênese, enquanto outras apresentam suas ações ainda incertas, como é o caso da interleucina (IL)-33. O objetivo deste estudo é avaliar o perfil de resposta inflamatória induzido por células de cultura estimuladas com a IL-33 e com o T. cruzi (parasito vivo e antígenos – Ags). Na etapa I, Ags obtidos de parasitos da cepa Y do T. cruzi em diferentes concentrações (0; 12,5; 25; 50; 100 e 200 µg/mL) foram utilizados para estimular células da linhagem J774, após 24h, sendo o sobrenadante coletado para a dosagem do TNF (fator de necrose tumoral) por imunoensaio enzimático (ELISA). Assim, a dose selecionada foi a de 100µg para estimular as células. Na etapa II, realizou-se o cultivo de células J774 adicionando 5x105 células/poço para o estímulo com antígeno. Na etapa III foram plaqueadas cerca de 1,25x105 células/poço utilizando1x106 formas tripomastigotas metaciclícas do T. cruzi como estímulo. Os estímulos seguiram o seguinte padrão: (i) cultura sem IL-33 e sem antígeno/T. cruzi; (ii) cultura com IL-33 (10 ng/ml) e sem antígeno/T. cruzi; (iii) cultura sem IL-33 com antígeno (100µg/mL) e T. cruzi; (iv) cultura com IL-33 (10ng/ml) e com antígeno (100µg/mL) e T. cruzi. As culturas foram avaliadas em diferentes tempos após os estímulos, sendo eles 0h, 24h e 48h e os sobrenadantes coletados para dosagem dos mediadores inflamatórios: TNF, IL-17 (interleucina 17), CCL2 (ligante 2 da quimiocina do grupo CC), IL-10 (interleucina 10), dosagem de nitrito pelo método de Griess e contagem de amastigotas. Observou-se diferenças na produção do TNF, IL-17, CCL2 para os grupos estimulados pelo antígeno ou pelo T. cruzi nos tempos de 24h e 48h. Para a citocina IL-10, essas diferenças foram observadas apenas nos grupos estimulados com o T. cruzi. Em relação ao nitrito, observou-se diferenças nos grupos estimulados com Ag ou T. cruzi paras os tempos 0h, 24h e 48h. O número de formas amastigotas foi maior nas células estimuladas com a citocina IL-33. De forma geral, tanto o antígeno quanto o T. cruzi vivo, induziu a produção de mediadores inflamatórios nas células J774 com 24h ou de 48h. A IL-33 mostrou-se importante nos eventos iniciais da infecção tanto em células estimuladas com o Ag quanto com o parasito vivo, bem como no controle da citocina IL-10 nos grupos infectados. Dessa forma, concluímos que a citocina IL-33 durante a infecção in vitro pelo T. cruzi, em cultura de células J774, participa na produção de mediadores inflamatórios e regulatórios.Item Piperine as therapeutic agent in paracetamol-induced hepatotoxicity in mice.(2022) Coelho, Aline Meireles; Queiroz, Isabela Ferreira; Perucci, Luiza Oliveira; Souza, Melina Oliveira de; Lima, Wanderson Geraldo; Silva, André Talvani Pedrosa da; Costa, Daniela CaldeiraHigh doses of paracetamol (APAP) can cause irreversible liver damage. Piperine (P) inhibits cytochrome P450, which is involved in the metabolism of various xenobiotics, including paracetamol. We evaluated the hepatoprotective effects of piperine with or without N-acetylcysteine (NAC) in APAP-induced hepatotoxicity. The mice were treated with two doses of piperine (P20 or P40) and/or NAC at 2 h after administration of APAP. The NAC+P20 and NAC+P40 groups showed a reduced area of necrosis, MMP-9 activity, and Casp-1 expression. Furthermore, the NAC+P20 group was the only treatment that reduced alanine aminotransferase (ALT) and increased the levels of sulfhydryl groups (-SH). In the NAC+P40 group, NLRP-3 expression was reduced. Aspartate aminotransferase (AST), thiobarbituric acid-reactive substances (TBARS), and IL-1β expression decreased in the NAC, NAC+P20, and NAC+P40 groups compared to the APAP group. The liver necrosis area, TNF levels, carbonylated protein, and IL-18 expression decreased in the P40, NAC, NAC+P20, and NAC+P40 groups compared to the APAP group. The cytokine IL-6 was reduced in all treatments. Piperine can be used in combination with NAC to treat APAP-induced hepatotoxicity.Item Plasmin and plasminogen prevent sepsis severity by reducing neutrophil extracellular traps and systemic inflammation.(2023) Silva, Juliana Priscila Vago da; Zaidan, Isabella; Perucci, Luiza Oliveira; Brito, Larissa Froede; Teixeira, Lívia Cristina Ribeiro; Silva, Camila Meirelles Souza; Miranda, Thaís Cristina de; Melo, Eliza Mathias; Bruno, Alexandre Santos; Queiroz Júnior, Celso Martins; Sugimoto, Michelle Adriane Amantéa; Tavares, Luciana Padua; Ferreira, Lais Cunha Grossi; Borges, Isabela Nascimento; Schneider, Ayda Henriques; Baik, Nagyung; Silva, André Talvani Pedrosa da; Ferreira, Raphael Gomes; Alves Filho, José Carlos Farias; Nobre Junior, Vandack Alencar; Teixeira, Mauro Martins; Parmer, Robert J.; Miles, Lindsey A.; Sousa, Lirlândia Pires deSepsis is a lethal syndrome characterized by systemic inflammation and abnormal coagulation. Despite therapeutic advances, sepsis mortality remains substantially high. Herein, we investigated the role of the plasminogen/plasmin (Plg/Pla) system during sepsis. Plasma levels of Plg were significantly lower in mice subjected to severe compared with nonsevere sepsis, whereas systemic levels of IL-6, a marker of sepsis severity, were higher in severe sepsis. Plg levels correlated negatively with IL-6 in both septic mice and patients, whereas plasminogen activator inhibitor-1 levels correlated positively with IL-6. Plg deficiency render mice susceptible to nonsevere sepsis induced by cecal ligation and puncture (CLP), resulting in greater numbers of neutrophils and M1 macrophages, liver fibrin(ogen) deposition, lower efferocytosis, and increased IL-6 and neutrophil extracellular trap (NET) release associated with organ damage. Conversely, inflammatory features, fibrin(ogen), and organ damage were substantially reduced, and efferocytosis was increased by exogenous Pla given during CLP- and LPS-induced endotoxemia. Plg or Pla protected mice from sepsis-induced lethality and enhanced the protective effect of antibiotics. Mechanistically, Plg/Pla– afforded protection was associated with regulation of NET release, requiring Pla-protease activity and lysine binding sites. Plg/Pla are important host-protective players during sepsis, controlling local and systemic inflammation and collateral organ damage.Item Pre-eclampsia is associated with reduced resolvin D1 and maresin 1 to leukotriene B4 ratios in the plasma.(2019) Perucci, Luiza Oliveira; Santos, Talita Adriana Pereira dos; Santos, Patrícia Campi; Teixeira, Lívia Cristina Ribeiro; Alpoim, Patrícia Nessralla; Gomes, Karina Braga; Sousa, Lirlândia Pires; Dusse, Luci Maria Sant'Ana; Silva, André Talvani Pedrosa daProblem: Omega-3 and omega-6 fatty acids can be endogenously converted into mediators with pro-inflammatory (eg, leukotriene B4/LTB4) or anti-inflammatory/ pro-resolving activities (eg, resolvin D1/RvD1 and maresin 1/MaR1). Recent data indicate an imbalance of LTB4 and MaR1 levels in pre-eclampsia (PE), but the relative production of these mediators, including RvD1, and the role of these mediators in the disease pathogenesis remain unclear. Therefore, this study aimed to investigate the plasma levels of LTB4, RvD1, and MaR1 in pregnant women with or without PE and non-pregnant controls and their association with clinical/laboratory parameters of PE women. Method of study: LTB4, RvD1, and MaR1 plasma levels were measured by competitive enzyme immunoassay in 19 non-pregnant, 20 normotensive pregnant, and 21 PE women. Results: Plasma concentrations of LTB4 were higher and RvD1 were lower in PE women than in normotensive pregnant women, who presented higher levels of LTB4 and similar levels of RvD1 to non-pregnant women. MaR1 levels did not differ among the groups. Pre-eclampsia women had decreased RvD1/LTB4 and MaR1/LTB4 ratios. Considering only the PE group, positive correlations were observed among all the mediators tested, between LTB4 and white blood cell count and between RvD1 and creatinine levels. However, all lipid mediators correlated negatively with body mass index before pregnancy. LTB4 also correlated negatively with maternal age. Conclusion: Our findings suggest that the PE state results in systemic overproduction of LTB4 in relation to RvD1 and MaR1, and that these lipid mediators may be involved with the disease pathogenesis.Item Protein restriction during pregnancy affects lung development and promotes oxidative stress and inflammation in C57 BL/6 mice offspring.(2022) Castro, Thalles de Freitas; Matos, Natália Alves de; Souza, Ana Beatriz Farias de; Costa, Guilherme de Paula; Perucci, Luiza Oliveira; Silva, André Talvani Pedrosa da; Cangussú, Silvia Dantas; Menezes, Rodrigo Cunha Alvim de; Bezerra, Frank SilvaObjectives: The present study aimed to evaluate the effects of maternal protein restriction during pregnancy on the lungs of 1-d and 31-d old offspring of C57BL/6 mice. Methods: The C57BL/6 mice (810 wk) were used for breeding. After pregnancy confirmation, female mice were randomly divided into a control group (CG) receiving a standard diet (22% protein) and a protein- restriction group (PRG) receiving a low-protein diet (6% protein). In the low-protein diet, protein was replaced by carbohydrate. After parturition, female mice that received the low-protein diet were fed the standard diet. Male offspring were euthanized 1 d and 31 d after birth for subsequent analysis. We evaluated the effects of a protein-restricted diet during gestation in pulmonary organogenesis, lung oxidative stress, and pulmonary inflammatory response of the offspring. Results: PRG mice 1 d after birth showed lower body and lung mass, length, relative mass, lung density, and erythrocyte count compared with CG mice. There was an increase in alveolar airspace density and a higher mean linear intercept (Lm), greater oxidative damage, and inflammation in PRG mice compared with CG mice. At 31 d after birth, PRG mice had lower body mass, length, and lung mass values compared with CG mice. PRG mice showed greater recruitment of inflammatory cells to the airways. In addition, there was increased collagen deposition in the lungs, altered inflammatory mediators, and greater oxidative damage compared with CG mice. Conclusions: Protein restriction during pregnancy reduces the body weight of offspring and promotes inflam- mation and oxidative stress, resulting in a simplification of the lung structure.Item The deleterious impact of exposure to different inhaled anesthetics is time dependent.(2022) Machado Júnior, Pedro Alves; Souza, Ana Beatriz Farias de; Castro, Thalles de Freitas; Perucci, Luiza Oliveira; Silva, André Talvani Pedrosa da; Cangussú, Silvia Dantas; Bezerra, Frank SilvaIn this study, the effects of exposure to isoflurane, sevoflurane and desflurane on the oxidative response and inflammation at different times was analyzed in the lungs of adult C57BL/6 mice. 120 animals were divided into 3 groups (n = 40): Isoflurane (ISO), Sevoflurane (SEV) and Desflurane (DES) and exposed to these anesthetics for 1 h (n = 10), 2 h (n = 10) and 3 h (n = 10), at a minimum alveolar concentration (MAC) equal to 1. The control group (CG) (n = 10) was exposed to ambient air. 24 h after the experimental protocol, the animals were euthanized and the bronchoalveolar lavage fluid (BALF), blood and lung tissue samples were collected. In the BALF, animals exposed to isoflurane for 2 h and 3 h showed a greater influx of leukocytes, especially macro- phages compared to the CG. The ISO3h had lower leukocyte counts in the peripheral blood compared to CG, ISO1h and ISO2h. There was an increase in CCL-2 levels in the ISO3h compared to the CG. Superoxide dismutase activity was higher in ISO1h compared to CG. The activity of catalase was higher in the ISO1h and ISO2h compared to the CG. The lipid peroxidation, as well as carbonylated protein were higher in the ISO3h compared to the CG (p < 0.05). Similar results were observed in the exposure of SEV and DES compared to inflammation and redox imbalance in different periods. This study demonstrated that time is a determinant to promote a local and systemic inflammatory response to different inhalational anesthetics in a healthy murine model.Item The imbalance in the relationship between inflammatory and regulatory cytokines during gestational toxoplasmosis can be harmful to fetuses : a systematic review.(2023) Santos, Priscilla Vilela dos; Toledo, Débora Nonato Miranda de; Souza, Débora Maria Soares de; Menezes, Tatiana Prata; Perucci, Luiza Oliveira; Silva, Zolder Marinho; Teixeira, Daniela Caldas; Vieira, Ed Wilson Rodrigues; Andrade Neto, Valter Ferreira de; Guimarães, Nathalia Sernizon; Silva, André Talvani Pedrosa daObjective: To evaluate the available information on inflammatory and regulatory plasma mediators in pregnant women (PW) diagnosed with toxoplasmosis. Source: The PubMed, Embase, Scopus, and Lilacs databases were evaluated until October 2022. Study eligibility criteria: This review was carried out following the PRISMA and registered on the PROSPERO platform (CRD42020203951). Studies that reported inflammatory mediators in PW with toxoplasmosis were considered. Evaluation methods: After excluding duplicate articles, two authors independently carried out the process of title and abstract exclusion, and a third resolved disagreements when necessary. The full text was evaluated to detect related articles. The extraction table was built from the following data: Author, year of publication, journal name and impact factors, country, study design, number of gestations and maternal age (years), gestational period, diagnosis of toxoplasmosis, levels of inflammatory markers, laboratory tests, and clinical significance. Methodological quality was assessed using Joanna Briggs Institute tools. Results: Of the 1,024 studies reported, only eight were included. Of the 868 PW included in this review, 20.2% were IgM+/IgG- and 50.8% were IgM-/IgG+ to T. gondii, and 29.0% uninfected. Infected PW presented higher plasma levels ofIL-5, IL-6, IL-8, IL-17, CCL5, and IL-10. Regarding the methodological quality, four studies obtained high quality. Data from this review pointed out the maintenance of the inflammatory pattern during pregnancy with a closely related to the parasite. Conclusion: Immune status in PW defined the course of the T. gondii infection, where the equilibrium between inflammatory and regulatory cytokines mitigated the harmful placenta and fetus effects.Item Upregulation of IL-33, CCL2, and CXCL16 levels in Brazilian pregnant women infected by Toxoplasma gondii.(2023) Santos, Priscilla Vilela dos; Toledo, Débora Nonato Miranda de; Guimarães, Nathalia Sernizon; Perucci, Luiza Oliveira; Andrade Neto, Valter Ferreira de; Silva, André Talvani Pedrosa daCongenital toxoplasmosis can cause neurological and eye damage, behavioral alterations, or death in fetuses or babies born to Toxoplasma gondii-infected women. Several pieces of evidence suggest that socioeconomic, environmental, and inflammatory patterns linked to the maternal immune response partly drive the pathogenesis of this disease. However, immunoregulation induced by T. gondii infection during gestation is not completely understood. The aim of this study was to assess the association between T. gondii seropositivity and concen- trations of plasma markers (CCL2, CXCL16, IL-17, and IL-33) in Brazilian pregnant women. Inflammatory markers were measured by immunoassays in the plasma of 131 pregnant women (13 to 46 years old). The prevalence of T. gondii infections was 45.8% (n = 60) in this population. The concentrations of CCL2, CXCL16, and IL-33 were higher in T. gondii-seropositive than in seronegative pregnant women, while the opposite was observed for IL-17 levels. In IgG+ women, a strong correlation between IL-17 and IL-33 (r = 0.7508, p = 0.0001) and a moderate correlation between CXCL16/IL-17 (r = 0.7319, p = 0.0001) and CXCL16/CCL2 (r = 0.3519, p = 0.0098) was observed. In uninfected women, a strong correlation was found between IL-17 and CXCL16 (r = 0.6779, p = 0.0001) but moderate between IL-17 and IL-33 (r = 0.4820, p = 0.0001). In summary, our data suggest that plasma upregulation of CCL2, CXCL16, and IL-33 might exert a potential protective role in the mother/fetus/parasite axis and, in addition, multiparous women are more likely to be infected with T. gondii than primiparous women.Item Zika virus induces oxidative stress and decreases antioxidant enzyme activities in vitro and in vivo.(2020) Almeida, Letícia Trindade; Ferraz, Ariane Coelho; Caetano, Camila Carla da Silva; Menegatto, Marília Bueno da Silva; Andrade, Ana Cláudia dos Santos Pereira; Lima, Rafaela Lameira Souza; Camini, Fernanda Caetano; Pereira, Samille Henriques; Pereira, Karla Yanca da Silva; Silva, Breno de Mello; Perucci, Luiza Oliveira; Silva, André Talvani Pedrosa da; Magalhães, José Carlos de; Magalhães, Cíntia Lopes de BritoThe first outbreak of Zika virus (ZIKV) infection in the Americas, especially in Brazil, was reported in 2015. Fever, headache, rash, and conjunctivitis are the common symptoms of ZIKV infection. Unexpected clinical outcomes, such as microcephaly and Guillain-Barré syndrome, have also been reported. The recent spread of ZIKV and its association with severe illness has created an urgent need to understand its pathogenesis and find potential therapeutic targets. Studies show that some viruses, including Flavivirus, trigger oxidative stress, which affects cellular metabolism, viral cycle, and pathogenesis. However, the role of oxidative stress in ZIKV infection needs to be investigated. Here, we analyzed ZIKV infection-triggered oxidative stress and modified antioxidant enzyme activities. U87-MG and HepG2 cells were infected to measure reactive oxygen species (ROS), malondialdehyde (MDA), and carbonyl protein levels, the activities of superoxide dismutase (SOD) and catalase (CAT), and the activation of nuclear factor erythroid 2p45-related factor 2 (Nrf2). ZIKV infection induced a significant increase in ROS, lipid peroxidation, and protein carbonylation products and a significant decrease in SOD and CAT activities accompanied by inhibition of Nrf2 activation in both cell lines. Further, MDA and carbonyl protein levels and SOD and CAT activities were evaluated in the brain and liver of ZIKV-infected C57BL/6 mice, and oxidative stress associated with antioxidant depletion was also found to occur in vivo. Together, our findings indicate the potential use of antioxidants as a novel therapeutic approach to Zika disease, and future studies in this direction are warranted.