VANESSA JACOB VICTORINO
Projetos de Pesquisa
Unidades Organizacionais
LIM/51 - Laboratório de Emergências Clínicas, Hospital das Clínicas, Faculdade de Medicina
3 resultados
Resultados de Busca
Agora exibindo 1 - 3 de 3
- Influence of Body Mass Index on Inflammatory Profile at Admission in Critically Ill Septic Patients(2015) ZAMPIERI, Fernando G.; JACOB, Vanessa; SILVA, Fabiano Pinheiro da; SOUZA, Heraldo P. deIntroduction. Inflammation is ubiquitous during sepsis and may be influenced by body mass index (BMI). We sought to evaluate if BMIwas associated with serumlevels of several cytokinesmeasured at intensive care unit admission due to sepsis. Methods. 33 septic patients were included. An array of thirty-two cytokines and chemokines was measured using Milliplex technology. We assessed the association between cytokine levels and BMI by generalized additive model that also included illness severity (measured by SAPS 3 score); one model was built for each cytokine measured. Results. We found that levels of epidermal growth factor, vascular endothelial growth factor, and interleukins 4, 5, and 13 were associated with BMI in a complex, nonlinear way, independently of illness severity. Higher BMI was associated with higher levels of anti-inflammatory interleukins. Conclusion. BMI may influence host response to infection during critical illness. Larger studies should confirm these findings.
conferenceObject Inflammatory and antioxidant response in obese septic shock patients(2013) VICTORINO, Vanessa Jacob; BARBEIRO, Hermes Vieira; BARBEIRO, Denise Frediani; SILVA, Fabiano Pinheiro; SOUZA, Heraldo PossoloThere is no consensus about the influence of obesity on sepsis. Hence, we evaluated the inflammatory and antioxidant response in obese patients (body mass index > 30) with septic shock compared to non-infected obese and non-obese septic patients. Blood samples were obtained from 27 critically ill patients admitted to ICUs in Clinics Hospital, Universidade de Sao Paulo. Cytokines were measured by ELISA Milliplex and antioxidant activity by colorimetric methods. There are small differences in the cytokine profiles in obese septic patients (n=6), compared to obese non-infected ones (n=10). Only FGF2, TGF-α, IFN-α2, IFN-{gamma}, IL-10, MCP-3, IL-13 and IL-15 presented significantly higher levels in septic patients. Interestingly, there was a marked increase in superoxide dismutase (SOD) and catalase (CAT) activity in erythrocytes from the septic group. Compared to their non-obese septic counterparts, septic obese patients presented significantly lower levels of FGF2, IL-4, TNF-β and VEGF. SOD activity was higher in this group, compared to non-obese patients. We concluded that obese patients with septic shock maintain cytokine levels similar to the ones observed in their non-obese counterparts, while increasing their antioxidant activity.- Sepsis Induces Telomere Shortening: a Potential Mechanism Responsible for Delayed Pathophysiological Events in Sepsis Survivors?(2016) OLIVEIRA, Naara Mendes; RIOS, Ester C. S.; LIMA, Thais Martins de; VICTORINO, Vanessa Jacob; BARBEIRO, Hermes; SILVA, Fabiano Pinheiro da; SZABO, Csaba; SORIANO, Francisco GarciaSepsis survivors suffer from additional morbidities, including higher risk of readmissions, nervous system disturbances and cognitive dysfunction, and increased mortality, even several years after the initial episode of sepsis. In many ways, the phenotype of sepsis survivors resembles the phenotype associated with accelerated aging. Since telomere shortening is a hallmark of aging, we investigated whether sepsis also leads to telomere shortening. Male balb/c mice were divided into two groups: the control group received 100 mu l of normal saline intraperitoneally (i.p.) and the sepsis group received 15 mg/kg of bacterial lipopolysaccharide i.p. After 48 h, animals were euthanized to collect blood, spleen and kidney. The human component of our study utilized blood samples obtained from patients in the trauma department and samples collected 7 d later in those patients who developed sepsis. Telomere length was measured by quantitative polymerase chain reaction. Since oxidative stress is a known inducer of telomere shortening, thiobarbituric acid-reactive substances and superoxide dismutase activity were analyzed to evaluate oxidative stress burden. Induction of endotoxemia in mice resulted in significant telomere shortening in spleen and kidney. Blood cells from patients who progressed to sepsis also exhibited a statistically significant reduction of telomere length. Endotoxemia in mice also induced an early-onset increase in oxidative stress markers but was not associated with a downregulation of telomerase protein expression. We conclude that endotoxemia and sepsis induce telomere shortening in various tissues and hypothesize that this may contribute to the pathogenesis of the delayed pathophysiological events in sepsis survivors.