Sepsis: integrating basic research and clinical research II

• Grant number: 11/20401-4
• Support type: Research Projects - Thematic Grants
• Duration: April 01, 2012 - September 30, 2017
• Field of knowledge: Health Sciences - Medicine
• Principal Investigator: Reinaldo Salomão
• Grantee: Reinaldo Salomão
• Home Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil
• Co-Principal Investigators: Ana Cristina Gales ; Ivan Hong Jun Koh
• Assoc. researchers: Eliezer Silva ; Flavia Ribeiro Machado ; Luciano Cesar Pontes de Azevedo ; Milena Karina Coló Brunialti ; Otelo Rigato Junior
• Associated grant(s): 16/12102-0 - 29th Annual Congress of the European Society of Intensive Care Medicine, AR.EXT
• Associated scholarship(s): 17/10523-1 - Study of the blood flow hemodynamics of the regional veins of the abdominal organs and its relation with macro and microcirculatory flows in sepsis, BP.IC; 16/13855-2 - Evaluation of energy and oxidative metabolism in peripheral blood mononuclear cells (PBMC) from septic patients, BP.DR; 15/21950-2 - Evaluation of CD39 and CD73 ectoenzymes expressed in lymphocytes, monocytes and neutrophils of septic patients, BP.IC; + associated scholarships 15/17109-0 - Evaluation of genes expression involved in Nod-like receptor (NLR) activation in PBMCs from sequential samples of patients with sepsis secondary to real-time array PCR pneumonia, BP.IC; 13/02265-1 - Characterization of the microcirculation dysfunction kinetics in sepsis, BP.PD; 12/19738-7 - A computational method for the analysis of tissue and microvascular changes in organs with sepsis using the Sidestream Dark FieldImaging (SDF) imaging technique, BP.DR - associated scholarships

Abstract

Sepsis is a major public health problem, with an estimated 400,000 cases / year in Brazil which cause about 200,000 deaths and costs about $ 20 billion annually. With complex pathogenesis, morbidity / mortality depends on factors of the infecting microorganism, the host immune response and appropriate therapeutic interventions. In this project we plan to integrate basic and clinical research in sepsis, focusing on the pathogenesis and development of intervention strategies, education and dissemination of knowledge. To succeed in integrating basic and clinical, we will maintain the structure of the previous project, based on three lines of research: epidemiological and clinical, for multicenter assessment of epidemiological data and evaluating the impact of interventions; clinical and experimental-interface: to evaluate the cellular regulatory mechanisms during sepsis and study of pathogenic factors of microorganisms isolated from patients; experimental studies: for evaluation of pathophysiological mechanisms and strategies for therapeutic intervention in sepsis. These lines are structured in three integrated lines of action: 1-clinical and epidemiological, we have established a network of hospitals that prospectively follow patients with sepsis, with storage of clinical and epidemiological and biological sample collection; 2-clinical and experimental interface: biological samples from patients and controls obtained from the hospital network will be transported and processed in a central laboratory of immunology and microbiology; 3 - Experimental Research: where new hypotheses and potential therapeutic targets will be evaluated. (AU)

Scientific publications

(7)

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

FERREIRA DA MOTA, NADIJANE VALERIA; COLO BRUNIALTI, MILENA KARINA; SANTOS, SIDNEIA SOUSA; MACHADO, FLAVIA RIBEIRO; ASSUNCAO, MURILLO; PONTES AZEVEDO, LUCIANO CESAR; SALOMAO, REINALDO. IMMUNOPHENOTYPING OF MONOCYTES DURING HUMAN SEPSIS SHOWS IMPAIRMENT IN ANTIGEN PRESENTATION: A SHIFT TOWARD NONCLASSICAL DIFFERENTIATION AND UPREGULATION OF FC gamma RI-RECEPTOR. Shock, v. 50, n. 3, p. 293-300, SEP 2018. Web of Science Citations: 1.

SHARMA, NARENDRA KUMAR; TASHIMA, ALEXANDRE KEIJI; COLO BRUNIALTI, MILENA KARINA; FERREIRA, EDEN RAMALHO; SOARES TORQUATO, RICARDO JOSE; MORTARA, RENATO ARRUDA; MACHADO, FLAVIA RIBEIRO; ASSUNCAO, MURILLO; RIGATO, OTELO; SALOMAO, REINALDO. Proteomic study revealed cellular assembly and lipid metabolism dysregulation in sepsis secondary to community-acquired pneumonia. SCIENTIFIC REPORTS, v. 7, NOV 15 2017. Web of Science Citations: 1.

ESQUERDO, K. F.; SHARMA, N. K.; BRUNIALTI, M. K. C.; BAGGIO-ZAPPIA, G. L.; ASSUNCAO, M.; AZEVEDO, L. C. P.; BAFI, A. T.; SALOMAO, R. Inflammasome gene profile is modulated in septic patients, with a greater magnitude in non-survivors. CLINICAL AND EXPERIMENTAL IMMUNOLOGY, v. 189, n. 2, p. 232-240, AUG 2017. Web of Science Citations: 9.

ALVES-JANUZZI, AMANDA BARBA; COLO BRUNIALTI, MILENA KARINA; SALOMAO, REINALDO. CD163 and CD206 expression does not correlate with tolerance and cytokine production in LPS-tolerant human monocytes. CYTOMETRY PART B-CLINICAL CYTOMETRY, v. 92, n. 3, SI, p. 192-199, MAY 2017. Web of Science Citations: 4.

NUCCI, LAURA A.; SANTOS, SIDNEIA S.; BRUNIALTI, MILENA K. C.; SHARMA, NARENDRA KUMAR; MACHADO, FLAVIA R.; ASSUNCAO, MURILLO; DE AZEVEDO, LUCIANO C. P.; SALOMAO, REINALDO. Expression of genes belonging to the interacting TLR cascades, NADPH-oxidase and mitochondrial oxidative phosphorylation in septic patients. PLoS One, v. 12, n. 2 FEB 9 2017. Web of Science Citations: 3.

SHARMA, NARENDRA KUMAR; SALOMAO, REINALDO. SEPSIS THROUGH THE EYES OF PROTEOMICS: THE PROGRESS IN THE LAST DECADE. Shock, v. 47, n. 1, 1, p. 17-25, JAN 2017. Web of Science Citations: 5.

DE ARAUJO, ORLEI RIBEIRO; SALOMAO, REINALDO; COLO BRUNIALTI, MILENA KARINA; BOURGUIGNON DA SILVA, DAFNE CARDOSO; SENERCHIA, ANDREZA ALMEIDA; DE MORAES COSTA CARLESSE, FABIANNE ALTRUDA; PETRILLI, ANTONIO SERGIO. Cytokine Kinetics in Febrile Neutropenic Children: Insights on the Usefulness as Sepsis Biomarkers, Influence of Filgrastim, and Behavior of the IL-23/IL-17 Pathway. Mediators of Inflammation, 2017. Web of Science Citations: 0.