RGD Reference Report - Transcriptional profiling of lipopolysaccharide-induced acute lung injury. - Rat Genome Database

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Transcriptional profiling of lipopolysaccharide-induced acute lung injury.

Authors: Jeyaseelan, S  Chu, HW  Young, SK  Worthen, GS 
Citation: Jeyaseelan S, etal., Infect Immun. 2004 Dec;72(12):7247-56.
RGD ID: 5135247
Pubmed: PMID:15557650   (View Abstract at PubMed)
PMCID: PMC529166   (View Article at PubMed Central)
DOI: DOI:10.1128/IAI.72.12.7247-7256.2004   (Journal Full-text)

Mortality associated with acute lung injury (ALI) induced by lipopolysaccharide (LPS) remains high in humans, warranting improved treatment and prevention strategies. ALI is characterized by the expression of proinflammatory mediators and extensive neutrophil influx into the lung, followed by severe lung damage. Understanding the pathogenesis of LPS-induced ALI is a prerequisite for designing better therapeutic strategies. In the present study, we used microarrays to gain a global view of the transcriptional responses of the lung to LPS in a mouse model of ALI that mimics ALI in humans. A total of 71 inflammation-associated genes were up-regulated in LPS-treated lungs, including a chemokine, LPS-induced CXC chemokine (LIX), whose role in the induction of ALI is unknown. Most of the inflammatory genes peaked at 2 h post-LPS treatment. Real-time reverse transcription-PCR confirmed the LPS-induced up-regulation of selected genes identified by microarray analysis, including LIX. The up-regulation of LIX, tumor necrosis factor alpha, and macrophage inflammatory protein 2 was confirmed at the protein level by enzyme-linked immunosorbent assays. To determine the role of LIX in the induction of ALI, we used both exogenous LIX and a LIX blocking antibody. Exogenous LIX alone elicited a neutrophil influx in the lungs, and the anti-LIX antibody attenuated the LPS-induced neutrophil accumulation in the lungs. Taken together, the results of our study demonstrate for the first time the temporal expression of inflammatory genes during LPS-induced ALI and suggest that early therapeutic intervention is crucial to attenuate lung damage. Moreover, we identified a role for LIX in the induction of ALI, and therefore LIX may serve as a novel therapeutic target for the minimization of ALI.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CXCL2HumanAcute Lung Injury  ISOCxcl2 (Mus musculus)mRNA and protein:increased expression:lungRGD 
CXCL5HumanAcute Lung Injury  ISOCxcl5 (Mus musculus)mRNA and protein:increased expression:lungRGD 
Cxcl2RatAcute Lung Injury  ISOCxcl2 (Mus musculus)mRNA and protein:increased expression:lungRGD 
Cxcl2MouseAcute Lung Injury  IEP mRNA and protein:increased expression:lungRGD 
Cxcl5MouseAcute Lung Injury  IEP mRNA and protein:increased expression:lungRGD 
Cxcl6RatAcute Lung Injury  ISOCxcl5 (Mus musculus)mRNA and protein:increased expression:lungRGD 

Objects Annotated

Genes (Rattus norvegicus)
Cxcl2  (C-X-C motif chemokine ligand 2)
Cxcl6  (C-X-C motif chemokine ligand 6)

Genes (Mus musculus)
Cxcl2  (C-X-C motif chemokine ligand 2)
Cxcl5  (C-X-C motif chemokine ligand 5)

Genes (Homo sapiens)
CXCL2  (C-X-C motif chemokine ligand 2)
CXCL5  (C-X-C motif chemokine ligand 5)


Additional Information