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1. Angiogenic and inflammatory markers in acute respiratory distress syndrome and renal injury associated to A/H1N1 virus infection.

Author

Bautista E, Arcos M, Jimenez-Alvarez L, García-Sancho MC, Vázquez ME, Peña E, Higuera A, Ramírez G, Fernández-Plata R, Cruz-Lagunas A, García-Moreno SA, Urrea F, Ramírez R, Correa-Rotter R, Pérez-Padilla JR, and Zúñiga J

Subjects
Acute Kidney Injury mortality, Acute Kidney Injury virology, Adult, Biomarkers metabolism, Chemokine CCL2 metabolism, Chemokine CXCL10 metabolism, Female, Humans, Influenza A Virus, H1N1 Subtype isolation & purification, Influenza, Human complications, Influenza, Human mortality, Male, Mexico epidemiology, Respiratory Distress Syndrome mortality, Respiratory Distress Syndrome virology, Survival Rate, Vascular Endothelial Growth Factor A metabolism, Acute Kidney Injury metabolism, Angiogenic Proteins metabolism, Inflammation metabolism, Influenza, Human metabolism, Neovascularization, Pathologic metabolism, Respiratory Distress Syndrome metabolism
Abstract

Acute kidney injury (AKI) is often associated to acute respiratory distress syndrome (ARDS) due to influenza A/H1N1 virus infection. The profile of angiogenic and inflammatory factors in ARDS patients may be relevant for AKI. We analyzed the serum levels of several angiogenic factors, cytokines, and chemokines in 32 patients with A/H1N1 virus infection (17 with ARDS/AKI and 15 ARDS patients who did not developed AKI) and in 18 healthy controls. Significantly higher levels of VEGF, MCP-1, IL-6, IL-8 and IP-10 in ARDS/AKI patients were detected. Adjusting by confusing variables, levels of MCP-1 ≥150 pg/mL (OR=12.0, p=0.04) and VEGF ≥225 pg/mL (OR=6.4, p=0.03) were associated with the development of AKI in ARDS patients. Higher levels of MCP-1 and IP-10 were significantly associated with a higher risk of death in patients with ARDS (hazard ratio (HR)=10.0, p=0.02; HR=25.5, p=0.03, respectively) even taking into account AKI. Patients with influenza A/H1N1 infection and ARDS/AKI have an over-production of MCP-1, VEGF and IP-10 possibly contributing to kidney injury and are associated to a higher risk of death., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Published
2013
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2. Seasonal and pandemic influenza H1N1 viruses induce differential expression of SOCS-1 and RIG-I genes and cytokine/chemokine production in macrophages.

Author

Ramírez-Martínez G, Cruz-Lagunas A, Jiménez-Alvarez L, Espinosa E, Ortíz-Quintero B, Santos-Mendoza T, Herrera MT, Canché-Pool E, Mendoza C, Bañales JL, García-Moreno SA, Morán J, Cabello C, Orozco L, Aguilar-Delfín I, Hidalgo-Miranda A, Romero S, Suratt BT, Selman M, and Zúñiga J

Subjects
DEAD Box Protein 58, DEAD-box RNA Helicases metabolism, Gene Expression Profiling, Gene Expression Regulation, Humans, Immunity genetics, Immunity immunology, Inflammation Mediators metabolism, Influenza, Human epidemiology, Intercellular Signaling Peptides and Proteins metabolism, Macrophages virology, Oligonucleotide Array Sequence Analysis, RNA, Messenger genetics, RNA, Messenger metabolism, Receptor, Interferon alpha-beta genetics, Receptor, Interferon alpha-beta metabolism, Receptors, Immunologic, Seasons, Suppressor of Cytokine Signaling 1 Protein, Suppressor of Cytokine Signaling 3 Protein, Suppressor of Cytokine Signaling Proteins metabolism, Chemokines biosynthesis, DEAD-box RNA Helicases genetics, Influenza A Virus, H1N1 Subtype physiology, Influenza, Human virology, Macrophages metabolism, Pandemics, Suppressor of Cytokine Signaling Proteins genetics
Abstract

Background: Infection with pandemic (pdm) A/H1N1 virus induces high levels of pro-inflammatory mediators in blood and lungs of experimental animals and humans., Methods: To compare the involvement of seasonal A/PR/8/34 and pdm A/H1N1 virus strains in the regulation of inflammatory responses, we analyzed the changes in the whole-genome expression induced by these strains in macrophages and A549 epithelial cells. We also focused on the functional implications (cytokine production) of the differential induction of suppressors of cytokine signaling (SOCS)-1, SOCS-3, retinoid-inducible gene (RIG)-I and interferon receptor 1 (IFNAR1) genes by these viral strains in early stages of the infection., Results: We identified 130 genes differentially expressed by pdm A/H1N1 and A/PR/8/34 infections in macrophages. mRNA levels of SOCS-1 and RIG-I were up-regulated in macrophages infected with the A/PR/8/34 but not with pdm A/H1N1 virus. mRNA levels of SOCS-3 and IFNAR1 induced by A/PR/8/34 and pdm A/H1N1 strains in macrophages, as well as in A549 cells were similar. We found higher levels of IL-6, TNF-α, IL-10, CCL3, CCL5, CCL4 and CXCL8 (p < 0.05) in supernatants from cultures of macrophages infected with the pdm A/H1N1 virus compared to those infected with the A/PR/8/34 strain, coincident with the lack of SOCS-1 and RIG-I expression. In contrast, levels of INF-α were higher in cultures of macrophages 48h after infection with the A/PR/8/34 strain than with the pdm A/H1N1 virus., Conclusions: These findings suggest that factors inherent to the pdm A/H1N1 viral strain may increase the production of inflammatory mediators by inhibiting SOCS-1 and modifying the expression of antiviral immunity-related genes, including RIG-I, in human macrophages., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Published
2013
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