Evidence for Monocyte Reprogramming in a Long-Term Postsepsis Study

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Gritte, Raquel Bragante ; Souza-Siqueira, Talita ; da Silva, Eliane Borges ; de Oliveira, Laiane Cristina dos Santos ; Borges, Rodrigo Cerqueira ; Alves, Heloisa H. de Oliveira ; Masi, Laureane Nunes ; Murata, Gilson Masahiro ; Gorjao, Renata ; Levada-Pires, Adriana Cristina ; Nogueira, Antonio Carlos ; Pithon-Curi, Tania Cristina ; de Azevedo, Ricardo Bentes ; Soriano, Francisco Garcia ; Curi, Rui ; Machado, Marcel Cerqueira Cesar

• Document type: Journal article
• Source: CRITICAL CARE EXPLORATIONS; v. 4, n. 8, p. 12-pg., 2022-08-01.

Abstract

OBJECTIVES:This study sought to identify monocyte alterations from septic patients after hospital discharge by evaluating gene expression of inflammatory mediators and monocyte polarization markers. It was hypothesized that sepsis reprograms the inflammatory state of monocytes, causing effects that persist after hospital discharge and influencing patient outcomes.DESIGN:The gene expression patterns of inflammatory receptors, M1 and M2 macrophage polarization markers, NLRP3 inflammasome components, and pro- and anti-inflammatory cytokines in monocytes were assessed.PATIENTS:Thirty-four patients from the University of S & atilde;o Paulo Hospital, during the acute sepsis phase (phase A), immediately after ICU discharge (phase B), and 3 months (phase C), 6 months (phase D), 1 year (phase E), and 3 years (phase F) after discharge, were included. Patients that died during phases A and B were grouped separately, and the remaining patients were collectively termed the survivor group.MEASUREMENTS AND MAIN RESULTS:The gene expression of toll-like receptor (TLR)2 and TLR4 (inflammatory receptors), NLRP3, NF kappa B1, adaptor molecule apoptosis-associated speck-like protein containing a CARD, caspase 1, caspase 11, and caspase 12 (NLRP3 inflammasome components), interleukin-1 alpha, interleukin-1 beta, interleukin-18, and high-mobility group box 1 protein (proinflammatory cytokines), interleukin-10 (anti-inflammatory cytokine), C-X-C motif chemokine ligand 10, C-X-C motif chemokine ligand 11, and interleukin-12p35 (M1 inflammatory polarization markers), and C-C motif chemokine ligand 14, C-C motif chemokine ligand 22, transforming growth factor-beta (TGF-beta), SR-B1, and peroxisome proliferator-activated receptor gamma (M2 anti-inflammatory polarization and tissue repair markers) was upregulated in monocytes from phase A until phase E compared with the control group.CONCLUSIONS:Sepsis reprograms the inflammatory state of monocytes, probably contributing to postsepsis syndrome development and mortality. (AU)

• FAPESP's process: 17/13715-9 - Inflammatory and epigenetic markers of prognosis of patients with sepsis after hospital discharge
• Grantee: Marcel Cerqueira Cesar Machado
• Support Opportunities: Regular Research Grants
• FAPESP's process: 18/09868-7 - Cellular and molecular mechanisms of insulin resistance and inflammation in obese Wistar rats and lean Goto-Kakizaki rats: causes and associations with diet and physical exercise
• Grantee: Rui Curi
• Support Opportunities: Research Projects - Thematic Grants
• FAPESP's process: 21/08624-0 - Post-COVID Sydrom: immunological sequelae after COVID-19 infection
• Grantee: Marcel Cerqueira Cesar Machado
• Support Opportunities: Regular Research Grants