Unknown,Transcriptomics,Genomics,Proteomics

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Inflammasome-regulated cytokines are critical mediators of lung injury in humans.

ABSTRACT: A microarray analysis involving whole blood samples isolated from critically ill patients in the medical intensive care unit at Brigham and Women's Hospital. Four groups of intubated subjects undergoing mechanical ventilation were recruited for the study: those with sepsis alone (Sepsis), those with sepsis + ARDS (se/ARDS), those with SIRS (SIRS), and those whithout sepsis, SIRS, or ARDS (untreated). Blood was obtained from patients on the day of admission (day 0) and 7 days later. RNA was isolated from the whole blood samples and microarrays were prepared to determine differential gene expression between the four groups. Total RNA obtained from whole blood samples of critically ill patients

ORGANISM(S): Homo sapiens

SUBMITTER: Judie Howrylak

PROVIDER: E-GEOD-32707 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Inflammasome-regulated cytokines are critical mediators of acute lung injury.

Dolinay Tamás T Kim Young Sam YS Howrylak Judie J Hunninghake Gary M GM An Chang Hyeok CH Fredenburgh Laura L Massaro Anthony F AF Rogers Angela A Gazourian Lee L Nakahira Kiichi K Haspel Jeffrey A JA Landazury Roberto R Eppanapally Sabitha S Christie Jason D JD Meyer Nuala J NJ Ware Lorraine B LB Christiani David C DC Ryter Stefan W SW Baron Rebecca M RM Choi Augustine M K AM

American journal of respiratory and critical care medicine 20120329 11

<h4>Rationale</h4>Despite advances in clinical management, there are currently no reliable diagnostic and therapeutic targets for acute respiratory distress syndrome (ARDS). The inflammasome/caspase-1 pathway regulates the maturation and secretion of proinflammatory cytokines (e.g., IL-18). IL-18 is associated with injury in animal models of systemic inflammation.<h4>Objectives</h4>We sought to determine the contribution of the inflammasome pathway in experimental acute lung injury and human ARD ...[more]

PMID: 22461369

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Project description:Expression data from CD8+ T cells and CD68+ monocytes from patients with hemophagocytic lymphohistiocytosis, sepsis, and persistent systemic inflammatory response syndrome Hemophagocytic lymphohistiocytosis (HLH) is a syndrome characterized by pathologic immune activation in which prompt recognition and initiation of immune suppression is essential for survival. Children with HLH have many overlapping clinical features with critically ill children with sepsis and persistent systemic inflammatory response syndrome (SIRS) in whom alternative therapies are indicated. To determine if plasma biomarkers could differentiate HLH from other inflammatory conditions and to better define a ‘core inflammatory signature’ of HLH, concentrations of inflammatory plasma proteins were compared in 40 patients with HLH to 47 pediatric patients with severe sepsis or SIRS. Seventeen of 135 analytes were significantly different in HLH plasma compared to SIRS/sepsis, including increased interferon-gamma (IFNg)-regulated chemokines CXCL9, CXCL10 and CXCL11. Further, a 5-analyte plasma protein classifier including these chemokines was able to differentiate HLH from SIRS/sepsis. Gene expression in CD8+ T cells and CD68+ monocytes from blood were also enriched for IFNg pathway signatures in peripheral blood cells from patients with HLH compared to SIRS/sepsis. This study identifies differential expression of inflammatory proteins as a diagnostic strategy to identify critically ill children with HLH. Further, comprehensive unbiased analysis of inflammatory plasma proteins and global gene expression demonstrates that IFNg signaling is uniquely elevated in HLH. In addition to demonstrating the ability of diagnostic criteria for HLH, sepsis and SIRS to identify groups with distinct inflammatory patterns, results from this study support the potential for prospective evaluation of inflammatory biomarkers to aid in diagnosis of and optimizing therapeutic strategies for children with distinctive hyperinflammatory syndromes.

Dataset Information

Inflammasome-regulated cytokines are critical mediators of lung injury in humans.

Publications

Inflammasome-regulated cytokines are critical mediators of acute lung injury.

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