HERMES VIEIRA BARBEIRO

Índice h a partir de 2011
14
Projetos de Pesquisa
Unidades Organizacionais
Instituto Central, Hospital das Clínicas, Faculdade de Medicina
LIM/51 - Laboratório de Emergências Clínicas, Hospital das Clínicas, Faculdade de Medicina

Resultados de Busca

Agora exibindo 1 - 10 de 12
  • article 3 Citação(ões) na Scopus
    Chronic Low or High Nutrient Intake and Myokine Levels
    (2023) SIERRA, Ana Paula Renno; FONTES-JUNIOR, Antonio Alves; PAZ, Ines Assis; SOUSA, Cesar Augustus Zocoler de; MANOEL, Leticia Aparecida da Silva; MENEZES, Duane Cardoso de; ROCHA, Vinicius Alves; BARBEIRO, Hermes Vieira; SOUZA, Heraldo Possolo de; CURY-BOAVENTURA, Maria Fernanda
    Inadequate nutrient availability has been demonstrated to be one of the main factors related to endocrine and metabolic dysfunction. We investigated the role of inadequate nutrient intakes in the myokine levels of runners. Sixty-one amateur runners participated in this study. The myokine levels were determined using the Human Magnetic Bead Panel from plasma samples collected before and after the marathon. Dietary intake was determined using a prospective method of three food records. The runners with lower carbohydrate and calcium intakes had higher percentages of fat mass (p < 0.01). The runners with a sucrose intake comprising above 10% of their energy intake and an adequate sodium intake had higher levels of BDNF (p = 0.027 and p = 0.031). After the race and in the recovery period, the runners with adequate carbohydrate intakes (g/kg) (>5 g/kg/day) had higher levels of myostatin and musclin (p < 0.05). The runners with less than 45% of carbohydrate of EI had lower levels of IL-15 (p = 0.015) and BNDF (p = 0.013). The runners with higher cholesterol intakes had lower levels of irisin (p = 0.011) and apelin (p = 0.020), and those with a low fiber intake had lower levels of irisin (p = 0.005) and BDNF (p = 0.049). The inadequate intake influenced myokine levels, which promoted cardiometabolic tissue repair and adaptations to exercise.
  • article 1 Citação(ões) na Scopus
    Exercise Induced-Cytokines Response in Marathon Runners: Role of ACE I/D and BDKRB2+9/-9 Polymorphisms
    (2022) SIERRA, Ana Paula Renno; GALAN, Bryan Steve Martinez; SOUSA, Cesar Augustus Zocoler de; MENEZES, Duane Cardoso de; BRANQUINHO, Jessica Lais de Oliveira; NEVES, Raquel Leao; ARATA, Julia Galanakis; BITTENCOURT, Clarissa Azevedo; BARBEIRO, Hermes Vieira; SOUZA, Heraldo Possolo de; PESQUERO, Joao Bosco; CURY-BOAVENTURA, Maria Fernanda
    Renin-angiotensin system (RAS) and kallikrein-kinin system (KKS) have a different site of interaction and modulate vascular tone and inflammatory response as well on exercise adaptation, which is modulated by exercise-induced cytokines. The aim of the study was to evaluate the role of ACE I/D and BDKRB2 +9/-9 polymorphism on exercise-induced cytokine response. Seventy-four male marathon finishers, aged 30 to 55 years, participated in this study. Plasma levels of exercise-induced cytokines were determined 24 h before, immediately after, and 24 h and 72 h after the Sao Paulo International Marathon. Plasma concentrations of MCP-1, IL-6 and FGF-21 increased after marathon in all genotypes of BDKRB2. IL-10, FSTL and BDNF increased significantly after marathon in the genotypes with the presence of the -9 allele. FSTL and BDNF concentrations were higher in the -9/-9 genotype compared to the +9/+9 genotype before (p = 0.006) and after the race (p = 0.023), respectively. Apelin, IL-15, musclin and myostatin concentrations were significantly reduced after the race only in the presence of -9 allele. Marathon increased plasma concentrations of MCP1, IL-6, BDNF and FGF-21 in all genotypes of ACE I/D polymorphism. Plasma concentrations of IL-8 and MIP-1alpha before the race (p = 0.015 and p = 0.031, respectively), of MIP-1alpha and IL-10 after the race (p = 0.033 and p = 0.047, respectively) and VEGF 72 h after the race (p = 0.018) were lower in II homozygotes compared to runners with the presence of D allele. One day after the race we also observed lower levels of MIP-1alpha in runners with II homozygotes compared to DD homozygotes (p = 0.026). Before the marathon race myostatin concentrations were higher in DD compared to II genotypes (p = 0.009). Myostatin, musclin, IL-15, IL-6 and apelin levels decreased after race in genotypes with the presence of D allele. After the race ACE activity was negatively correlated with MCP1 (r = -56, p < 0.016) and positively correlated with IL-8, IL-10 and MIP1-alpha (r = 0.72, p < 0.0007, r = 0.72, p < 0.0007, r = 0.47, p < 0.048, respectively). The runners with the -9/-9 genotype have greater response in exercise-induced cytokines related to muscle repair and cardioprotection indicating that BDKRB2 participate on exercise adaptations and runners with DD genotype have greater inflammatory response as well as ACE activity was positively correlated with inflammatory mediators. DD homozygotes also had higher myostatin levels which modulates protein homeostasis.
  • article 16 Citação(ões) na Scopus
    Septic shock in older people: a prospective cohort study
    (2013) SILVA, Fabiano Pinheiro da; ZAMPIERI, Fernando Godinho; BARBEIRO, Denise Frediani; BARBEIRO, Hermes Vieira; GOULART, Alessandra Carvalho; TORGGLER FILHO, Francisco; VELASCO, Irineu Tadeu; CRUZ NETO, Luiz Monteiro da; SOUZA, Heraldo Possolo de; MACHADO, Marcel Cerqueira Cesar
    Background: Septic shock is the first cause of death in Intensive Care Units. Despite experimental data showing increased inflammatory response of aged animals following infection, the current accepted hypothesis claims that aged patients are immunocompromised, when compared to young individuals. Results: Here, we describe a prospective cohort study designed to analyze the immune profile of this population. Conclusion: Older people are as immunocompetent as the young individual, regarding the cytokines, chemokines and growth factors response to devastating infection.
  • article 13 Citação(ões) na Scopus
    Time Course and Role of Exercise-Induced Cytokines in Muscle Damage and Repair After a Marathon Race
    (2021) SOUSA, Cesar Augustus Zocoler de; SIERRA, Ana Paula Renno; GALAN, Bryan Steve Martinez; MACIEL, Jaqueline Fernanda de Sousa; MANOEL, Richelieau; BARBEIRO, Hermes Vieira; SOUZA, Heraldo Possolo de; CURY-BOAVENTURA, Maria Fernanda
    Endurance exercise induces an increase in the expression of exercise-induced peptides that participate in the repair and regeneration of skeletal muscles. The present study aimed to evaluate the time course and role of exercise-induced cytokines in muscle damage and repair after a marathon race. Fifty-seven Brazilian male amateur marathon finishers, aged 30-55 years, participated in this study. The blood samples were collected 24 h before, immediately after, and 24 and 72 h after the Sao Paulo International Marathon. The leukogram and muscle damage markers were analyzed using routine automated methodology in the clinical laboratory. The plasma levels of the exercise-induced cytokines were determined using the Human Magnetic Bead Panel or enzyme-linked immunosorbent assays [decorin and growth differentiation factor 15 (GDF-15)]. A muscle damage was characterized by an increase in plasma myocellular proteins and immune changes (leukocytosis and neutrophilia). Running the marathon increased interleukin (IL)-6 (4-fold), IL-8 (1.5-fold), monocyte chemoattractant protein-1 (2.4-fold), tumor necrosis factor alpha (TNF-alpha) (1.5-fold), IL-10 (11-fold), decorin (1.9-fold), GDF-15 (1.8-fold), brain-derived neurotrophic factor (BDNF) (2.7-fold), follistatin (2-fold), and fibroblast growth factor (FGF-21) (3.4-fold) plasma levels. We also observed a reduction in musclin, myostatin, IL-15, and apelin levels immediately after the race (by 22-36%), 24 h (by 26-52%), and 72 h after the race (by 25-53%). The changes in BDNF levels were negatively correlated with the variations in troponin levels (r = -0.36). The variations in IL-6 concentrations were correlated with the changes in follistatin (r = 0.33) and FGF-21 (r = 0.31) levels after the race and with myostatin and irisin levels 72 h after the race. The changes in IL-8 and IL-10 levels had positive correlation with variation in musclin (p < 0.05). Regeneration of exercise-induced muscle damage involves the participation of classical inflammatory mediators, as well as GDF-15, BDNF, follistatin, decorin, and FGF-21, whose functions include myogenesis, mytophagia, satellite cell activation, and downregulation of protein degradation. The skeletal muscle damage markers were not associated to myokines response. However, BDNF had a negative correlation with a myocardial damage marker. The classical anti-inflammatory mediators (IL-10, IL-8, and IL-6) induced by exercise are associated to myokines response immediately after the race and in the recovery period and may affect the dynamics of muscle tissue repair.
  • article 54 Citação(ões) na Scopus
    An increase in mean platelet volume after admission is associated with higher mortality in critically ill patients
    (2014) ZAMPIERI, Fernando G.; RANZANI, Otavio T.; SABATOSKI, Viviane; SOUZA, Heraldo Possolo de; BARBEIRO, Hermes; DA NETO, Luiz Monteiro Cruz; PARK, Marcelo; SILVA, Fabiano Pinheiro da
    Background: Platelet activation and consumption are common in critically ill patients and are associated with poorer prognosis. Mean platelet volume is a simple surrogate for platelet activation, with higher MPV being associated with worse clinical condition on a large array of clinical diagnoses. We therefore aimed to investigate associations between changes in platelet count and mean platelet volume (MPV) with prognosis and inflammatory cytokine values in critically ill patients. Methods: This study prospectively included 84 critically ill patients. Patients were stratified into four groups according to proportional changes in MPV (Delta MPV24h) and platelet count (Delta Plat(24h)) in the first 24 hours after admission. Mortality between groups was compared using the chi(2) test. Logistic regression was performed using hospital mortality as outcome and Simplified Acute Physiology Score (SAPS 3), Delta Plat(24h) and Delta MPV24h as covariates. Concentrations of the following inflammatory mediators were measured using Miliplex (R) technology: IL1 beta, IL6, IL8, IL10, epidermal growth factor, vascular endothelial growth factor, TNF alpha and IFN alpha. Cytokine concentrations were compared between groups using the Kruskal-Wallis test with Bonferroni correction. Results: Patients in whom MPV increased and platelet count decreased had higher mortality rates (46%). According to logistic regression, Delta MPV24h was independently associated with increased mortality (OR 1.28 per 1% increase; 95% CI 1.08 to 1.48). No strong associations between inflammatory mediators and changes in MPV and platelet count were found. Conclusion: An increase in MPV after admission to an ICU is independently associated with higher hospital mortality.
  • article 1 Citação(ões) na Scopus
    Short-term Obesity Worsens Heart Inflammation and Disrupts Mitochondrial Biogenesis and Function in an Experimental Model of Endotoxemia
    (2022) PETRONI, Ricardo Costa; OLIVEIRA, Suelen Jeronymo Souza de; FUNGARO, Thais Pineda; ARIGA, Suely K. K.; BARBEIRO, Hermes Vieira; SORIANO, Francisco Garcia; LIMA, Thais Martins de
    Cardiomyopathy is a well-known complication of sepsis that may deteriorate when accompanied by obesity. To test this hypothesis we fed C57black/6 male mice for 6 week with a high fat diet (60% energy) and submitted them to endotoxemic shock using E. coli LPS (10 mg/kg). Inflammatory markers (cytokines and adhesion molecules) were determined in plasma and heart tissue, as well as heart mitochondrial biogenesis and function. Obesity markedly shortened the survival rate of mouse after LPS injection and induced a persistent systemic inflammation since TNF alpha, IL-1 beta, IL-6 and resistin plasma levels were higher 24 h after LPS injection. Heart tissue inflammation was significantly higher in obese mice, as detected by elevated mRNA expression of pro-inflammatory cytokines (IL-1 beta, IL-6 and TNF alpha). Obese animals presented reduced maximum respiratory rate after LPS injection, however fatty acid oxidation increased in both groups. LPS decreased mitochondrial DNA content and mitochondria biogenesis factors, such as PGC1 alpha and PGC1 beta, in both groups, while NRF1 expression was significantly stimulated in obese mice hearts. Mitochondrial fusion/fission balance was only altered by obesity, with no influence of endotoxemia. Obesity accelerated endotoxemia death rate due to higher systemic inflammation and decreased heart mitochondrial respiratory capacity.
  • article 0 Citação(ões) na Scopus
    Antimicrobial peptides and other potential biomarkers of critical illness in SARS-CoV-2 patients with acute kidney injury. AMPAKI-CoV study
    (2024) SANTOS, Lucas Ferreira Theotonio dos; BARBEIRO, Hermes Vieira; BARBEIRO, Denise Frediani; SOUZA, Heraldo Possolo de; SILVA, Fabiano Pinheiro da
    Antimicrobial peptides (AMPs) constitute a complex network of 10-100 amino acid sequence molecules widely distributed in nature. While over 300 AMPs have been described in mammals, cathelicidins and defensins remain the most extensively studied. Some publications have explored the role of AMPs in COVID-19, but these findings are preliminary, and in vivo studies are still lacking. In this study, we report the plasma levels of five AMPs (LL-37, alpha-defensin 1, alpha-defensin 3, beta-defensin 1, and beta-defensin 3), using the ELISA technique (MyBioSource, San Diego, CA, United States, kits MBS2601339 (beta-defensin 1), MBS2602513 (beta-defensin 3), MBS703879 (alpha-defensin 1), MBS706289 (alpha-defensin 3), MBS7234921 (LL37)), and the measurement of six cytokines (tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, interleukin-10, interferon-gamma, and monocyte chemoattractant protein-1), through the magnetic bead immunoassay Milliplex (R) and the MAGPIX (R) System (MilliporeSigma, Darmstadt, Germany, kit HCYTOMAG-60 K (cytokines)), in 15 healthy volunteers, 36 COVID-19 patients without Acute Kidney Injury (AKI) and 17 COVID-19 patients with AKI. We found increased levels of alpha-defensin 1, alpha-defensin 3 and beta-defensin 3, in our COVID-19 population, when compared to healthy controls, along with higher levels of interleukin-6, interleukin-10, interferon-gamma, and monocyte chemoattractant protein-1. These findings suggest that these AMPs and cytokines may play a crucial role in the systemic inflammatory response and tissue damage characterizing severe COVID-19. The levels of alpha-defensin 1 and alpha-defensin 3 were significantly higher in COVID-19 AKI group in comparison to the non-AKI group. Furthermore, IL-10 and the product IL-10 x IL-1B showed excellent performance in discriminating AKI, with AUCs of 0.86 and 0.88, respectively. Among patients with COVID-19, AMPs may play a key role in the inflammation process and disease progression. Additionally, alpha-defensin 1 and alpha-defensin 3 may mediate the AKI process in these patients, representing an opportunity for further research and potential therapeutic alternatives in the future. The activation of antimicrobial peptides is induced by the infiltration of SARS-CoV-2 into the epithelial cells. Alpha-defensins exhibit a positive correlation with renal injury, whereas beta-defensin 3 is associated with pulmonary impairment. The question of whether these peptides exert a causal influence or serve as modulators of the pathological pathways remains contentious. Moreover, the ensuing immune reaction escalates the concentrations of interleukin-10 (IL-10).image
  • article 1 Citação(ões) na Scopus
    Hypertonic solution-induced preconditioning reduces inflammation and mortality rate
    (2019) PIMENTEL, Rosangela Nascimento; PETRONI, Ricardo Costa; BARBEIRO, Hermes Vieira; BARBEIRO, Denise Frediani; ANDRADE, Mariana Macedo; ARIGA, Suely Kumini; SORIANO, Francisco Garcia
    BackgroundDysregulated inflammatory response is common cause of organ damage in critical care patients. Preconditioning/tolerance is a strategy to prevent exacerbated inflammation. The aim of this study is to analyze hypertonic saline 7.5% as a potential inducer of preconditioning that protect from a lethal dose of LPS and modulates systemic inflammatory profile in mice.MethodsMale Balb/C mice received intravenous (i.v.) injections of Hypertonic solution (NaCl 7.5%) (0.8ml) for 3days, on day 8th was challenged with LPS 15mg/kg. Controls with Saline 0.9%, urea and sorbitol were performed. Microarray of mRNA expression was analyzed from HS versus saline from macrophages to identified the pathways activated by HS.ResultsHS preconditioning reduced mortality after LPS injection as well reduced the cytokines release in plasma of the animals challenged by LPS. In order to check how HS induces a preconditioning state we measured plasma cytokines after each HS infusion. Repeated HS injections induced a state of preconditioning that reprograms the inflammatory response, resulting in reduced inflammatory cytokine production. A microarray of mRNA demonstrated that Hypertonic solution increased the expression of several genes in special Mapkbp1 and Atf3.Conclusionhypertonic solution induces preconditioning/tolerance reducing mortality and inflammatory response after LPS challenge.
  • article 2 Citação(ões) na Scopus
    Transcriptome analysis of six tissues obtained post-mortem from sepsis patients
    (2023) SILVA, Fabiano Pinheiro da; GONCALVES, Andre Nicolau Aquime; DUARTE-NETO, Amaro Nunes; DIAS, Thomaz Luescher; BARBEIRO, Hermes Vieira; BREDA, Cristiane Naffah Souza; BREDA, Leandro Carvalho Dantas; CAMARA, Niels Olsen Saraiva; NAKAYA, Helder I.
    Septic shock is a life-threatening clinical condition characterized by a robust immune inflammatory response to disseminated infection. Little is known about its impact on the transcriptome of distinct human tissues. To address this, we performed RNA sequencing of samples from the prefrontal cortex, hippocampus, heart, lung, kidney and colon of seven individuals who succumbed to sepsis and seven uninfected controls. We identified that the lungs and colon were the most affected organs. While gene activation dominated, strong inhibitory signals were also detected, particularly in the lungs. We found that septic shock is an extremely heterogeneous disease, not only when different individuals are investigated, but also when comparing different tissues of the same patient. However, several pathways, such as respiratory electron transport and other metabolic functions, revealed distinctive alterations, providing evidence that tissue specificity is a hallmark of sepsis. Strikingly, we found evident signals of accelerated ageing in our sepsis population.
  • article 0 Citação(ões) na Scopus
    Effects of CRAMP on the gut-brain axis in experimental sepsis
    (2024) BRUZAFERRO, Ewerton Vinicius Macarini; LIMA, Thais Martins de; ARIGA, Suely Kubo; BARBEIRO, Denise Frediani; BARBEIRO, Hermes Vieira; SILVA, Fabiano Pinheiro da
    The collaboration between the microbiota, mucosa, and intestinal epithelium is crucial for defending against pathogens and external antigens. Dysbiosis disrupts this balance, allowing pathogens to thrive and potentially enter the bloodstream, triggering immune dysregulation and potentially leading to sepsis. Antimicrobial peptides like LL-37 and CRAMP are pivotal in innate immune defense. Their expression varies with infection severity, exhibiting a dual pro- and anti-inflammatory response. Understanding this dynamic is key to comprehending sepsis progression. In our study, we examined the inflammatory response in CRAMP knockout mice post-cecal ligation and puncture (CLP). We assessed its impact on brain tissue damage and the intestinal microbiota. Our findings revealed higher gene expression of S100A8 and S100A9 in the prefrontal cortex of wild-type mice versus CRAMP- knockout mice. This trend was consistent in the hippocampus and cerebellum, although protein concentrations remained constant. Notably, there was a notable increase in Escherichia coli, Lactobacillus spp., and Enterococcus faecalis populations in wild-type mice 24 h post-CLP compared to the CRAMP-deficient group. These results align with our previous data suggesting that the absence of CRAMP may confer protection in this sepsis model.