RGD Reference Report - Role of CC chemokines (macrophage inflammatory protein-1 beta, monocyte chemoattractant protein-1, RANTES) in acute lung injury in rats. - Rat Genome Database

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Role of CC chemokines (macrophage inflammatory protein-1 beta, monocyte chemoattractant protein-1, RANTES) in acute lung injury in rats.

Authors: Bless, NM  Huber-Lang, M  Guo, RF  Warner, RL  Schmal, H  Czermak, BJ  Shanley, TP  Crouch, LD  Lentsch, AB  Sarma, V  Mulligan, MS  Friedl, HP  Ward, PA 
Citation: Bless NM, etal., J Immunol 2000 Mar 1;164(5):2650-9.
RGD ID: 68880
Pubmed: PMID:10679105   (View Abstract at PubMed)

The role of the CC chemokines, macrophage inflammatory protein-1 beta (MIP-1 beta), monocyte chemotactic peptide-1 (MCP-1), and RANTES, in acute lung inflammatory injury induced by intrapulmonary deposition of IgG immune complexes injury in rats was determined. Rat MIP-1 beta, MCP-1, and RANTES were cloned, the proteins were expressed, and neutralizing Abs were developed. mRNA and protein expression for MIP-1 beta and MCP-1 were up-regulated during the inflammatory response, while mRNA and protein expression for RANTES were constitutive and unchanged during the inflammatory response. Treatment of rats with anti-MIP-1 beta Ab significantly decreased vascular permeability by 37% (p = 0.012), reduced neutrophil recruitment into lung by 65% (p = 0.047), and suppressed levels of TNF-alpha in bronchoalveolar lavage fluids by 61% (p = 0.008). Treatment of rats with anti-rat MCP-1 or anti-rat RANTES had no effect on the development of lung injury. In animals pretreated intratracheally with blocking Abs to MCP-1, RANTES, or MIP-1 beta, significant reductions in the bronchoalveolar lavage content of these chemokines occurred, suggesting that these Abs had reached their targets. Conversely, exogenously MIP-1 beta, but not RANTES or MCP-1, caused enhancement of the lung vascular leak. These data indicate that MIP-1 beta, but not MCP-1 or RANTES, plays an important role in intrapulmonary recruitment of neutrophils and development of lung injury in the model employed. The findings suggest that in chemokine-dependent inflammatory responses in lung CC chemokines do not necessarily demonstrate redundant function.

Disease Annotations    
Acute Lung Injury  (IMP,ISO)

Gene Ontology Annotations    

Biological Process

Molecular Function

Objects Annotated

Genes (Rattus norvegicus)
Ccl4  (C-C motif chemokine ligand 4)

Genes (Mus musculus)
Ccl4  (chemokine (C-C motif) ligand 4)

Genes (Homo sapiens)
CCL4  (C-C motif chemokine ligand 4)

Objects referenced in this article
Gene Ccl5 C-C motif chemokine ligand 5 Rattus norvegicus

Additional Information