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Rescue Of Dysfunctional Autophagy By Peptide IDR-1018 Attenuates Hyperinflammatory Phenotype Of Cystic Fibrosis Cells (RNA-seq)


ABSTRACT: Genome-wide gene expression was measured in peripheral blood mononuclear cells (PBMCs) from patients with cystic fibrosis (CF) after treatment in vitro with the flagellin protein fliC, and/or synthetic peptide IDR-1018 to assess patterns of gene expression. The patterns of gene expression suggest that CF cells have a hyperinflammatory phenotype including dysfunctional autophagy processes. The synthetic peptide IDR-1018 attentuates this hyperinflammatory phenotype. Total RNA was obtained from PBMCs obtained from CF patients after treatment with the fliC flagellin protein (that is known to play a role in CF lung inflammation), and/or the peptide IDR-1018 that has anti-inflammatory properties. Comparison of genes and pathways affected by these treatments indicated the role of autophagy process in CF disease.

ORGANISM(S): Homo sapiens

SUBMITTER: Christopher Fjell 

PROVIDER: E-GEOD-35394 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Rescue of dysfunctional autophagy attenuates hyperinflammatory responses from cystic fibrosis cells.

Mayer Matthew L ML   Blohmke Christoph J CJ   Falsafi Reza R   Fjell Chris D CD   Madera Laurence L   Turvey Stuart E SE   Hancock Robert E W RE  

Journal of immunology (Baltimore, Md. : 1950) 20121221 3


A hallmark feature of cystic fibrosis (CF) is progressive pulmonary obstruction arising from exaggerated host proinflammatory responses to chronic bacterial airway colonization. The mechanisms for these heightened inflammatory responses have been only partially characterized, hampering development of effective anti-inflammatory therapies. The aim of this study was to identify and validate novel dysfunctional processes or pathways driving the hyperinflammatory phenotype of CF cells using systems  ...[more]

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