Increased grp78 transcription is correlated to reduced tlr4 transcription in patients surviving sepsis

Autor(es)

Stan, R. C. ^{[1, 2]} ; Bonin, C. Pinto ^[1] ; Porto, R. ^[3] ; Soriano, F. G. ^{[3, 4]} ; de Camargo, M. M. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Inst Biomed Sci, Sao Paulo - Brazil

^[2] Cantacuzino Mil Med Res Dev Natl Inst, Bucharest - Romania

^[3] Univ Sao Paulo, Univ Hosp, Sao Paulo - Brazil

^[4] Univ Sao Paulo, Sch Med, Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: CLINICAL AND EXPERIMENTAL IMMUNOLOGY; v. 198, n. 2 AUG 2019.
• Citações Web of Science: 0

Resumo

Regulated transcriptional readthrough during stress maintains genome structure and ensures access to genes that are necessary for cellular recovery. A broad number of genes, including of the bacterial sensor Toll-like receptor 3 (TLR-4), are markedly transcribed on initiating the systemic inflammatory response. Here we study the transcriptional patterns of tlr4 and of its modulator grp78 during human sepsis, and establish their correlations with the outcome of patients. We measured the daily tlr4 and grp78 RNA expression levels in peripheral blood of septic patients, immediately after admission to intensive care, and modeled these RNA values with a sine damping function. We obtained negative correlations between the transcription of tlr4 and grp78 RNA in the survivor group. In contrast, such relation is lost in the deceased patients. Loss of transcriptional homeostasis predicted by our model within the initial 4 days of hospitalization was confirmed by death of those patients up to 28 days later. (AU)

• Processo FAPESP: 11/51778-6 - Estudo funcional da via Unfolded Protein Response em linfócitos B humanos: hipogamaglobulinemia primária como modelo de disfunção da UPR
• Beneficiário: Maristela Martins de Camargo
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 08/54811-1 - Regulacao da sinalizacao por lps em linfocitos b de equinos.
• Beneficiário: Maristela Martins de Camargo
• Modalidade de apoio: Auxílio à Pesquisa - Regular